Acta anaesth. Scandinav. 1958, 2, 37-43.

POSITIVE-PRESSURE RESPIRATOR TREATMENT O F SEVERE PULMONARY

INSUFFICIENCY I N T H E NEWBORN INFANT

A CLINICAL R E P O R T

BY

FRANCIS BENSON, OLOV CELANDER, GORAN HAGLUND, LARS NILSSON, LEIF PAULSEN and LARS RENCK

Pulmonary insufficiency is a major cause of death in early neonatal life. The insufficiency of gas exchange is commonly caused by atelectasis of the lungs -congenital or the result of aspiration. Another group is caused by the so-called hyaline-membrane syndrome as described in detail by H. C. MILLER and M. H. JENNISON ( 195O)ls, E.L.POTTER ( 1952y2 and by R.E.L.NEsBITT and G.W. ANDERSON (1956)20. In the latter condition the new-born infant is generally observed to be normal and with good respiration for up to several hours after delivery. Then progressive dyspnoea is noted. Respiratory frequency increases from 40 up to 100-150-200 per minute. Mortality, as reported by W.BLYSTAD et al. (1951)*, E.L.POTTER (1952)22 and by P.KARLBERG et al. (1954)15, is high and is caused by a vicious circle of muscular exhaustion, hypoxia and accumulation of metabolites.

P. KARLBERG et al. ( 1954)15, W. BLYSTAD ( 1956)5 and H. C. MILLER et al. ( 1957)19 have confirmed the clinical diagnose of the hyaline-membrane syn- drome by laboratory analyses.

Chest radiographs show a normal picture just after delivery. When clinical symptoms develop, the radiographic findings change as illustrated by I. MESCHAN et al. (1953)17, H.G.PETTERSON and M.E.PENDELTON (1955)21 and by G. CURRARINO and F. M. SILVERMAN (1 957) 6. The lungs show the “ground-glass” appearance with widespread recticulogranular densities, mostly in the central parts.

The pathogenesis of the hyaline-membrane syndrome is disputed and a definite diagnosis rests upon the autopsy findings.

From the Children’s Hospital, Gothenburg, Sweden. Recieved December 30, 1957.

38 BENSON, CELANDER, HAGLUND, NILSSON, PAULSEN AND RENCK

SEVERE PULMONARY INSUFFICIENCY IN THE NEWBORN 39

20 -. 600- 600

5 200

ro - - 400 -- 4M -- -. 200

537-09.21 $E& G r /

Fig. 2.-Case 1, details of the “metabolic history”.

CASE REPORTS

Case 1. (1884/57. EE.).-First child of a 38-year-old woman with slight hypertension and oedema during pregnancy. Clear amniotic fluid 12 hours before delivery. Normal delivery of full-term girl after 12 hours’ labour. Body weight 2970 g. Good cry and colour. Two hours later, signs of respiratory insufficiency-cyanosis and hyperpnoea. Suction of mucus from mouth and pharynx was performed, and oxygen treatment was started. The child did not improve and was sent to the Medical Clinic of the Children’s Hospital. Here she was observed to be in an extremely bad general condition with deep cyanosis and no audible breathing sounds. The child was flaccid. Heart frequency 160 per minute. She was hurried to the Emergency Clinic. Here the patient was at once intubated intratra- cheally, and manual artificial respiration was given with the Y-piece described by G. HACLUND (1951)’O. Blood samples and radiographs could not be taken before treatment

40 BENSON, CELANDER, HAGLUND, NILSSON, PAULSEN AND RENCK

Fig. 3.-Case 1. (1) On admission, after immediate intubation. Widespread central atelec- tasis of the reticulogranular pattern with coarser peripheral densities.

(2) After 2 days respirator treatment. Almost complete regression. (3) First day without respirator. Recurrence of atelectasis on both sides. (4) Last day in hospital. Clear lungs.

was started. Suction of the trachea and upper bronchial tree gave no result. After 5 minutes of manual artificial respiration with 60% oxygen there was a slight improvement. Spon- taneous respiration began (frequency 85-100/min.) but was insufficient to maintain the general condition for more than about one minute. Now it was decided to instigate active treatment with the intratracheal positive-pressure respirator constructed by G. HAGLUND and A. WALDINCER (1955). Tracheotomy was performed 4 hours after delivery. Indications and techniques were those outlined by P.A.HOLINCER et al. (1954)’ and by G.HACLUND (1955 and 1957)14,13.

Details of the respirator treatment are given in figure 1 and the “metabolic history” in figure 2, while figure 3 shows some radiographs. The tracheostoma was closed on the 12th day. The patient was discharged on the 17th day; examination immediately before discharge showed no abnormal signs.

Case 2. (1982/57. B.).-Full-term male child. Body weight 3550 g. Cyanotic when delivered. Large amounts of mucus and green-coloured amniotic fluid in mouth and

SEVERE PULMONARY INSUFFICIENCY IN THE NEWBORN 41

pharynx. Improvement after pharyngial suction. Unchanged general condition with light cyanosis for 24 hours. Then progressive dyspnoea, increasing cyanosis and flaccidity. Radio- graphs showed widespread atelectasis. Respirator treatment begun 35 hours after delivery and continued for 13 days. Discharged on the 19th day; examination on that day showed no abnormal signs.

Case 3. (2000/57. M.).-Full-term male child. Body weight 3720 g. Good cry and respiration during the first 12 hours. Then hyperpnoea (increasing up to 200/min.), cyanosis and indrawing of thorax on inspiration. Positive radiographic findings. Respirator treat- ment begun 24 hours after delivery, and continued for 8 days. The tracheostoma was closed on the 13th day. Transferred to the medical ward on the 25th day because of feeding troubles. Discharged 3 weeks later; examination on the day of discharge showed no ab- normal signs.

DISCUSSION

Cases 1 and 3 showed the typical features of the so-called hyaline-membrane syndrome. In case 2 the symptoms were mainly due to aspiration, but the possibility of a combination with the hyaline-membrane syndrome cannot be excluded. The clinical appearance of our cases before the institution of treat- ment was definitely one of acute life-threatening pulmonary insufficiency.

In their excellent review on treatment of aspiralion, D. M. LrrTLE and R. M. TOVELL ( 1948)l6 clearly outlined the technique of suction of the mouth, pharynx and upper bronchial tree. In the treatment of the hyaline-membrane syndrome, P. KARLBERG et al. ( 1954)15 tried high humidity and increased oxygen tension in incubators. In some cases, the same authors gave hypothermia a trial. A. BLOXSOM ( 1950)3 tried active respirator treatment with iron-lung technique, and I. DONALD (1953)’, and R.F.GODDARD et al. (1953)8 attempted positive- pressure respiration through an endotracheal tube. The results obtained are difficult to evaluate from their papers. In describing the patient’s initial general condition an accepted terminology is lacking.

Concerning the radiographic diagnosis of the hyaline-membrane syndrome the densities may, in our opinion, be coarser. l’his is an experience gained in other cases of hyaline-membrane syndrome treated conservatively and con- firmed at autopsy.

At the Emergency Clinic (a report on the Emergency Clinic was given by G.HAGLUND (1957)9), intense work has been done to reach a standard respi- rator method suited to the newborn infant as reported by G.HAGLUND (1955 and 1957)12913,14. The basis of this treatment is the laboratory controls as outlined by P.ASTRUP et al. (1954)l. Clinical experience has taught us that capillary-blood samples are sufficient to provide adequate information of pH, pC02, total CO, and bicarbonate. Series of arterial or venous blood samples in newborn infants are practically impossible. Adequate respirator treatment of the newborn infant is impossible without close laboratory control. Bed-side observations are inadequate to assess the effect of treatment.

42 BENSON, CELANDER, HAGLUND, NILSSON, PAULSEN AND RENCK

As one of the aims of treatment is to expand the lungs, a high positive pres- suie is needed. A large minute volume is necessary for the maintenance of this high pressure, and to counterbalance the hyperventilating effect extra carbon dioxide must be given in the inspiratory air. Intravenous curare is given initially to avoid the danger of the patient breathing against the respirator. Without curare an extremely high pressure is sometimes needed to force the patient into the rhythm of the respirator, involving a considerable risk of lung damage. To facilitate the respirator treatment and bronchial toilet, tracheotomy is the method of choice. A complete report of this method of respirator treat- ment of the newborn infant is in preparation.

In our cases, we have observed a tendency to metabolic acidosis combined with the respiratory insufficiency, and in some situations we have found “half- way” correction with bicarbonate or lactate of benefit. We have aimed at a low normothermia to keep metabolism low. We have seen no reason to lower the body temperature beyond 35” C.

I t is interesting to note that we found little or no mucus in the trachea and upper bronchial tree during the first 12-24 hours after tracheotomy, even in case 2. After this initial delay, there is an increased amount of bronchial mucus for 3-6 days, during which time clinical improvement of the patient occurs.

To diminish the risk of tracheo-bronchial damage we have interrupted the respirator treatment as soon as the patient can do without it, even though manual positive-pressure respiration may be necessary for very short periods within the next two or three days.

During the post-respirator period we observed that the chest radiographs, u hich had been clear during the last part of the respirator-treatment period became more or less cloudy in a few hours (fig. 3). The spontaneous respiratory frequency is increased for a couple of days before the whole situation approaches normal (fig. 1). The infant must be carefully observed and the whole set-up kept ready for immediate re-use if necessary.

SUMMARY

Successful respirator treatment in three consecutive cases of severe pul- monary insufficiency in newborn infants is reported. The outlines of the team- work and the methods are given.

Addendum.

Three follow-up examinations of each infant have been made during the first five months of life in order to assess their general condition and psycho-motor development. Nothing abnormal was discovered (March 1, 1958).

SEVERE PULMONARY INSUFFICIENCY IN THE NEWBORN 43

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