1. Seventeen cases of sclerema neonatorum were observed during a period of 3 years and 9 months. Of these 17, sixteen were premature by weight. 2. Septicaemia was present in six, respiratory infection in four, and previous operative interference
Specimens from four cases of sclerema neonatorum were studied by light and electron microscopy. The connective tissue bands of the cutis and subcutis were thickened and alternated with loosely distributed bands in broad, distended areas of basal subs
In non-trachestomised patients of tetanus neonatorum adoption of semiprone position and continuous intragastric drip led to a marked decrease in the rate of aspiration and a six-fold decrease in the rate of chest infections as compared with the patie
Birth asphyxia is an insult to the fetus or newborn due to failure to breath or breathing poorly, leads to decrease oxygen perfusion to various organs. According to WHO, 4 million neonatal deaths occurred each year due to birth asphyxia. Our goal was
We presented an unusual case of negligent homicide by thorax compression, which is the expanded concept of traumatic asphyxia. A 58-year-old man was restrained in the prone position by six prison officers. They were ordered by their superiors to cont
Cardiac abnormalities in birth asphyxia were first recognised in the 1970s. These include (i) transient tricuspid regurgitation which is the commonest cause of a systolic murmur in a newborn and tends to disappear without any treatment unless it is a
IndianJ' Pediat.42: 42, 237, 1975
OF A S P H Y X I A N E O N A T O R U M *
Dibrug ar h Asphyxia neonatorum or birth asphyMa is an acute emergency which requires urgent resuscitation. It is a form of suffocation due to factors originating either in the mother or the foetus which affect neonatal respir~ttion. Often all the vital processes are depressed, including respiration. T h e condition may be sudden or subacute, transient or prolonged. Wilson and Wilton (1955) classified this condition into two groups: Infants who breathed and then the respiration stopped (secondary asphyxia) and those who had not breathed at all (primary asphyxia).
Maternal disease such as anaemia, hypotension, bleeding, toxaemia, tetanic contraction of t h e uterus.
Diseases of the placenta, such as infarction, prolapse cord, knot in cord, a n t e p a r t u m haemorrhage.
Effect of obstetric analgesia and general anaesthetic.
Peripheral causes Aspiration of meconium amnii or (1) mucous into the tracheobronchial tree.
Weakness of the thoracic muscles or t r a u m a to the thoracic cage. Prematurity.
In order that the scheme of resuscitation be logical, the anaesthetist must have an understanding of the cau~al factors. T h e r e are various classifications of causes (Lea and Atkinson 1968, Cook 1958). A convenient one is given below:
Central Causes (1) Abnormality in the C.N.S. in general and respiratory centre in particular. (2) Damage to the C.N.S. or respiratory centre due to t r a u m a in childbirth. Intraventricular haemorrhage and rupture of ependyreal vessels are the other traumatic causes (Donald 1960). *From the Department o| Anaesthesiology, Assam Medical College Hospital, Dibrugarh. Received on March 16, 1974.
Iatrogenic causes (1) I.V. oxytocin and obstetric analgesia: Foetal asphyxia after oxytocin therapy has been reported. There are various reports of asphyxia caused by spinal epidural analgesia. (2)
Para.cervical analgesia: Para-cervical block tends to cause foetal asphyxia. Drugs having a quinidine-like action cause severe bradycardia.
Supine hypotension: Countney (1970) reported a few deaths after supine hypotension. It was also remarked that undiagnosed supine hypotension is occasionally a cause of foetal asphyxia. L u m l e y et al. (1970) found an inverse relationship between the
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time taken to deliver in caesarian section (C.S.) and the foetal pH. Secondly, foetal pH is proportional to the degree of supine hyootension. This accounts for the poor condition of some babies after an apparently uncomplicated C.S.
is limited in obesity, hydramnios or if the foetus moves quickly. The sound may disappear at the peak of uterine contraction.
Movement produced by the foetal heart is recorded by a beam
of ultra sound of low acoustic energy on the mother's skin which is then transmitted by a transducer.
Diagnosis For many years intermittent recording of the foetal heart sounds (F.H.S.) with a stethoscope and detection of meconium in the liquor have been the only methods used for the diagnosis of asphyxia. As these have certain limitations, continuous electronic recording of the F.H.S. and measurement of foetal pH have been considered to be of better diagnostic value.
Foetal bloodpH A conical endoscope is pushed through the cervix till it reaches the foetus. A small area of the skin is visualised and cleaned with a swab and then sprayed with ethyl chloride to have reflex hyperaemia. A small nick is made with a guarded blade and a few drops of blood (0.2-0.5 ml.) is collected in a glass capillary tube containing heparin and measured by the Astrup pH metre. A pH value of 7.3 is regarded as the lower limit of the normal range. Values o f 7,20-7.24 denote pre-acidosis which is suggestive of foetal hypoxia. I f the pH comes down to 7.2 in the Ist stage of labour then G.S. is advised. I f the patient is in the 2nd stage then forceps are recommended for early delivery.
Continuous recording ofF H.S. (1) Abdominal method (Phonocardiography). A microphone is strapped over the mother's abdomen and the F.H.S. is recorded by a galvanometer, Its value
(3) Indirect Joetal electrocardiography.
Electrodes of the E.C.G. are attached to the mother's abdominal wall.
Intrauterine method. Direct E,C.G. electrodes are put through the dilated cervix after rupture of the membranes and the F.H.S. are recorded, the most accurate method.
Evaluation The simplest method for it is the Apgar scoring (Apgar 1953), but the llne of demarcation between different grades is difficult to define. Sixty seconds after birth, disregarding the cord and placenta, observations are made on the heart rate, respiration, colour, muscle tone and reflex activity. Each sign is given a score of 0, l or 2. T he best score is 10 and the worst is 0. The score has the advantage of being based on physical signs. The score is repeated at 5 minutes. An interval of 60 seconds was cboosen by Apgar because at this time she got low scores for asphyxia in her series, Serial evaluation provides valuable information about the progress. Each record should be attached to the case sheet. The most important of the scores is the time to sustained respiration (T.S.R.). This is more valuable than recording of breathing time or cry (Craford 1959).
B A R U A H - - M A N A G E M E N T OF A S P H Y X I A N E O N A T G R U M
Stage of respiratory depression (Asphyxia livida). The neonate is bluish white, with sluggish reflex activity The heart rate is below 100/min. and there is no respiratory effort. He requi~es active resuscitation. Stage of circulatory depression (Asphyxia pallida). T h e neonate is white with no reflex activity and the heart rate is slow or absent. Donald (1960) suggested the term foetal shock for this infant who requires very quick energetic resuscitation.
Stage of mild dtpression. T h e r e is an a t t e m p t at respiration; the heart rate is about 100/rain. and the body is pinkish blue. T h e infant also requires
resuscitation. These stages are more arbitrary, artificial and have limited meaning. Brown (1959) stressed that disturbances in circulatory and respiratory function cannot be normally separated.
Sequelae T h e after effects of anoxia are not limited to immediate life. They may present later with cerebral palsy, mental deterioration, epilepsy and unusual behaviour. Asphyxia may be associated with intracranial haemorrhage due to vascular congestion and compression of the cord by the foetal head. T h e r e m a y be impaired liver function, low coagulation time, low prothrombin level and fibrinolysis. T h e next is the problem o f hyaline membrane disease.
Procedure of Apgar scoring Assessment is best made by some one other than the person who conducted the
delivery. He should get all the information about drug therapy in pregnancy and labour and the mother's general health. As the head is born in vertex presentation the attendant should wipe or aspirate excess mucous and debris from the nares and oropharynx. A clock with a large second hand should be started after complete delivery of the infant. T h e infant is put on a warm flat surface and the head lowered 15-30 degrees at a convenient height. A quick over all examination is made to exclude gross congenital malformations. T h e infant is wrapped loosely with a warm dry sterile cover. T h e time o f first gasp, cry and sustained respiration are noted. I f there is no respiratory movement, the heart sound is listened to. One should not wait at this stage to complete one minute if the heart sound is not heard. Both cardiac massage and ventilation are to be started at once. After one minute if the condition is satisfactory, the infant is turned to a head up position and the 5-minute score is completed. Others prefer lateral and horizontal positions as the head low position hampers diaphragmatic movement and increases cerebral congestion. T h e r e can be no doubt that the infant must be placed close to the anaesthetist even though he takes no active part in the treatment. T h e heart beat is tile sing]e most important factor for assessment. Brown (1959) remarked that the newborn is tolerant of hypoxia but n~t ischaemia. Severe hypoxia can be treated but the outcome of circulatory failure is often doubtful. Apgar scoring teaches disciplined rapid assessment before resuscitation and is a valuable source of statistics for comparison o f obstetric techniques and anaesthetic
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resuscitatory methods but m a y be confusing unless regularly used. It is also time consuming.
majority of infants fall into this category and require no resuscitation at 1 m i n u t e after birth. H o w e v e r , they m u s t be
assessed again at 5 minutes as they m a y have some distress again.
Ambient temperature. During assessment and resuscitation, p a r t i c u l a r attention must be given to the prevention o f heat loss by the infant. The infant, p a r t i c u l a r l y his head, should be covered with a w a r m dry sheet. T h e environmental t e m p e r a t u r e should be m a i n t a i n e d by an external source of heat. Care must be taken in the use of undiffused r a d i a n t heat which can,badly burn the skin o f any infant in peripheral circulatory failure. Servo-controlled r a d i a n t w a r m t h m i g h t prove the best way to maintain the infant's body t e m p e r a t u r e during resuscitation.
Mucus extraction. During the initial minute o f observation, gentle nasal and pharyngeal suction with a soft catheter which has a single hole and mucus t r a p is recommended. Although blockage to the u p p e r airways with mucus m a y lead to respiratory difficulties, the value of mucus extraction lies as much in its stimulus to respiration and it affords an opportunity to check for anatomical abnormalities which m a y cause respiratory difficulties. Secondly, stimulation of the p h a r y n x m a y cause reflex b r a d y e a r d i a and breada holding. Formerly, milking of the trachea towards the m o u t h to remove the secretions was done. N o w it is obsolete. When a suction machine is used, the pressure should not be more than 25 cm o f H , O. I t is m a n d a t o r y to hold the head low till the cord is cut.
Gastric lavage. T h e contents of the stomach must be aspirated and lavage is to be done gently with n o r m a l saline. This will prevent chances of aspiration to the lungs. Mild depression (Apgar score 7--10). T h e
Moderately depressed infants ( Apgar Score 3-6). At 1 minute and in the absence of u p p e r airway obstruction, these infants should have oxygen or oxygen-enrlched (40-50 per cent) air blown on to the face through a mask. This cold stimulus and oxygen sometimes i m p r o v e the infant's condition. An A m b u bag is attached to the face and ventilated at a rate of 18-22/mln. with a pressure not m o r e than 30 era. HsO. I f the infaht does not i m p r o v e with it within one minute then it is better to examine the larynx. After this procedure, the infant m a y start breathing. I f not, then intermittent positive pressme respiration (I.P.P.R.) is started t h r o u g h on endotracheal tube. Barcroft (1946) showed that in the normal infant sensory stimuli from the periphery, u p p e r respiratory tract, joints and muscles play a large p a r t in the initiation of respiration. In the depressed infant such a stimulus is of less value.
Severely depressed infants (Apgar score 0-2). These infants require immediate help. An endotracheal tube should be inserted, after proper pharyngcal suction, and then the lungs are inflated. T h e usual response to this t r e a t m e n t is a sudden i~crease in the intensity and r a t e o f the heart sounds; the infant rapidly becomes pink; respiratory efforts start; and the muscle tone returns. I f it does not, external cardiac massage is carried out.
Indications for intubations: Any b a b y born apnoeic or flaccid with a slow weak h e a r t
BARUAH--MANAGEMENT OF ASPHYXIA NEONATORO~
rate, suspicion o f inhalation of mucus, meconium, or liquor amnii, premature infant born in a poor condition; full-term infant born severely asphyxiated and in a state of shock; full-term iiafant who has not started regular respiration at one minute.
Types of tubes: T h e various endotracheal tubes used are: Magill '00' (3 mm.), Cole tube, Portsmouth Ruplex tube, and St. T h o m a s ' ttospital tube (plastic tube 3 ram. • 6"). T h e last two are sterile and disposable. The tube should be kept for a considerable time as re-insertion is difficult. At no time should blind intubation be tried. Barrie's (1963) m e t h o d o f I P.P.R. for resuscitative purposes is most ideal, but high concentrations of oxygen may cause atelectasis and hyaline m e m b r a n e disease. For prevention, Donald (1954) had suggested assisted or augmented respiration whenever possible and that more than 40 per cent oxygen should not be used. M o u t h to mouth or nose ventilation can also be tried. O T H E R METHODS OF OXYGENATION
I. Oxygen insufftation. A small nasal catheter is put close to the tracheal opening and oxygen flow at 2.1/m. is supplied. This provides a tactile stimulus. Secondly it changes intrabronchial pressure. 1. lntragastric oxygenation. Oxygen is given t h r o u g h a double lumen oxygen catheter through a Wolf bottle. It is not a good method and has the following drawbacks: T h e efficiency of the gastric mucosa to absorp oxygen is doubted; unwanted intragastric distension increases chances of rupture of the oesophagus and stomach; it does not help 2n expansion of the lungs; it causes more trauma to the mucosa; and it does not supply oxygen to the lungs at once.
Twin channel airway oxygenation. This is a double channel curved airway. A gadget is attached over the m o u t h to make it airtight. 4.
Hyperbaric oxygenation. The basic idea is t h a t at high pressure plasma oxygen is increased. The infant is put in a special c h a m b e r at 3 atmospheric pressures. It is very costly and does not effectively remove carbon dioxide from the lungs. Nursing in
the chamber is problematic.
Maternal oxygen administration. In ease of complicated labour, oxygen therapy is rational. But prolonged therapy causes vasoconstriction of the placental vessels and retention of carbon dioxide and lactic acid. This effect can be treated fully with theophyllin or perphyllion (theopyllin, papavarine and atropine). 6.
Other methods such as nasal catheter, funnel or mask have no place in apnoea of the newborn. DRUG THERAPY
1. Buffer infusion. This is indicated most when the p H is below 7.15. A mixture of 2 ml. of 40 per cent tris buffer with 10 ml. of I0 per cent dextrose which becomes 7 per cent of buffer with 8 per cent glucose has been recommended. It is injected slowly through the umbilical vein within 2 minutes of delivery. In the absence of tris buffer, sodium bicarbonate 8.4 per cent (5 ml.) with 5-10 per cent dextrose is injected. T h e total does is 4 ml./kg, weight. It is repeated in 5-10 minutes when necessary. Higher doses in a severely acidotic infant cause no abnormality in plasma osmolality. A further dose is given on the basis of the biochemical assessment of acidosis.
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Administration of bicarbonate solution to the acidotic mother in labour is equally beneficial.
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doses ofacetylcholine given I.V. choice is perphyllon.
T he next
Cortisone. Dexamethasone 1 mg. by I.V.
or I.M. may be of value in case of severe asphyxia. Th e rationale for its use is to reduce intracranial pressure; to decrease capillary fragility; and to reduce pulmonary inflammatory reaction to aspirated material.
3. Electrolytes. For a few days after birth the infant has poor control of plasma osmolality. There is often a gross swing of electrolyte concentration with hyponatraemia, hyperkalaemia, hypocalcaemia, h y p o -o r hyper-glycaemia. Correction of the electrolytes reduces the infant's tendency to convulse and makes the neurological findings easier to interpret 4.
T h e y have little or no value
and often cause harm when given to asphyxiated babies. Nalorphine 0.5 mg. or naloxan (0.2-0.3rag) is of value in counteracting the effects of maternal sedation with morphine, diamorphiqe or pethidine. Barrie et al. (1962) showed that lobeline and amiphenazole have no place here. However, nikethamide (50-125 nag.) or vanillic acid diethylamine (10-25 rag.) can be tried. Vasopressors are rarely used. In foetal shock, Young (1956) a~d Brown (1959) suggested noradrenaline in 5 per cent dextrose through the umbilical vein. 5. Vasodilators. In hypoxia, pulmonary vasoconstriction and then right to left shunt occur. They both cause respiratory distress and metabolic acidosis. Workers have now found good results with small
Carbon dioxide therapy. Formerly 5 per cent carbon dioxide was used as a respiratory stimulant. It has little use. 7. Nitrogen and oxygen therapy. Whenever an infant requires prolonged oxygenation, some workers used to add 60 per cent nitrogen to prevent atelectasis of the lung. HYPOTHERMIA
The management of severe hypoxia is helped by hypothermia (25-30~ and a small transfusion of oxygenated blood. EXTERNAL
Slowing of the heart rate or its absence in spite of ventilation is an ominous sign and is the indication for cardiac massage. This is carried out by compressing the heart between the chest wall and vertebral column. The index and middle finger are placed to the left of the lower sternal border. The chest wall is depressed approximately 2 cm. and then released at a rate of about 80/rain. Every 4-5 seconds the fingersshould be lifted and the chest listened to for the heart beat. One should stop the massage when the heart rate is more than 100/min. Milstein's (1963) method is to apply pressure with the thumb
and counter pressure by other fingers on the back. AUGMENTED RESPIRATION Phrenic nerve stimulation was practised earlier but now-a-days most workers like the trigger type of ventilator. The question when to stop ventilation cannot have a simple answer. Useful
BARUAH--MANAGEMENT OF ASPHYXIA NEONATORUM
criteria are regular respiration, maintain-
anaesthetist is more t h a n t h a t
nance of good colour and regular heart beat after correction of metabolic acidosis. It is easy to ventilate for l to 2 hours. It is better to continue ventilation till the opinion of an experienced neonatal paediatrician or paediatric neurologist is obtained.
m e m b e r s of the team. H e should be tile leader of the resuscitative effort and must
Conclusions Resuscitation is to be commenced before birth. T h e anaesthetist can do m u c h to mitigate or a v o i d i n t r a p a r t u m asphyxia. Measures directed to this angle include pre-operative infusion, maintenance o f blood pressure, a d m i n i s t r a t i o n of oxygen and avoidance of unnecessary drugs. Till the cord is separated the b a b y should be held head down and the airway must be cleared. I t is evident that the evaluation of the neonate, the choice a n d application of therapeutic measures to be taken, d e m a n d both c o m m o n sense and experience. All persons attending the delivery--obstetrician, anaesthetist, paediatrician and midwife should be conversant with the scheme of resuscitation. I n t u b a t i o n of the
d e m a n d s considerable skill and care and should preferably be performed by an anaesthetist. The presence o f a congenital a b n o r m a l i t y must be dealt with quickly. Acute hypoxia in the neonate is related to neurological sequelae in the adult. A dead infant is better t h a n a crippled one. T h u s supreme i m p o r t a n c e should be paid to sustained anoxia. An a p p a r e n t l y n o r m a l b a b y or a fully recovered one should not be left unobserved. He may present some problems within a short time. T h e role of the
be able to guide the steps taken others.
I am thankful to the Superintendent, Assam Modical College Hospital, Dibrugarh, for his kind permission to publish the paper. I also thank Dr. R.K. Borkotoky, Professorand tiead of the Department of Obstetrics and Gynaecology, Assam Medical College Hospital, Dibrugarh, for his kind help.
Apgar, V. (1953). A proposal for a new method of evaluation of the new born infant. Curt. Res. Anaesth. 32, 260. Barcroft, J. (1946). Researches of prenatal life. Springfield, Charles C. Thomas. Barrie, H., Cotton, D and Wilson, B.D.R. (1962). Respiratory stimulant in the new born. Lancet, 2,
742. Barrie, H. (1963). Resuscitation of the new born. Lancet, 1, 650. Brown, R.J.K. (1959). Brit. 07. Anaesth. 32, 106. Quoted from Emergel~cy Anaetbesia by Thronton, H.L. and Knight, P.F.E.A. Ltd., London (1965). Cook, C.D.(1958). Paraeervieal block. ALT.S.ff. Med. 58, 372. Countney, L. (1970). Supine hypotension syndrome during caesarean section. Brit. Med. 07. 1, 797. Craford, J.S. (1956). Some aspects of obstetric analgesia, Part II (The u s e of relaxant drugs). Brit. 07. Anaesth. 28, 154. Craford, J.S. (1959). Principles and Practice of Obstetric Anaesthesia. Blackwdl Scientific Publication. Oxford. Donald, I. (1954). Atelectasis neonatorum. 07. Obst. and Gynae. Brit. Emp. 61, 725. Donald, I. (1960). Classification of asphyxia, Brit. 07. Anaesth. 32, 106. Lea, L.A., Atkinson, R.B. (1968). A Synopsis of Anaesthesia 6th Ed. Bristol, ffohn Wright & Son Ltd., Bristol.
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Lumley, J. Renu, P. Newman, W. and Wood, C. (1970). Blood volume in pregnancy. A,ner. jT" Obst. & Gynae 103 847. Milstein, B.B. 11963). Cardiac Arrest a n d Resuscitation. 1st Ed. Lloyd Luke ( M~dical Book~ Ltd) London.
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