ACQUIRED ASPHYXIA This is also called atelectasis pulmonum and is encountered in premature and debilitated children. We differentiate according to the Onset an early and a late form of asphyxia. (Concerning the latter see also the chapter on prematurity and debility).
The etiology of this form of asphyxia is rather complex.
I. General debility with which all the functions are quantitatively and qualitatively impaired and a high degree of somnolence exists; with this, through a lingering carbonic acid intoxication, paralysis of the respiratory centre results (Finkelstein).
II. Cerebral diseases; especially injuries in the region of the me dulla, front birth-traumata (haemorrhages?); also congenital hydro cephalus.
III. Pulmonary affections (aplasia of the lungs, white pneu monia); also congenital struma or hyperplasia of the thymus which leads to compression of the trachea.
IV. A yielding thoracic wall and costal cartilages, as well as a poorly developed respiratory musculature in premature children.
V. Acute fatty degeneration of the newborn (Buhl's disease) which in the absence of hfemorrhages can be masked through the symptom of asphyxia.
VI. Underfeeding (Budin) as well as overfeeding (Henry) are held responsible as etiological factors in cases of asphyxia in premature children.
The course of asphyxia occurring soon after birth, especially in premature and debilitated children, is usually as follows: the children usually slumber apathetically, without demanding nourishment, and are noticeably quiet. The face is at times slightly puffed and slight oedema occurs on the extremities, especially on the backs of hands and feet. The temperature is subnormal. The breathing, tolerable at first, be comes more superficial and irregular; now quicker and now interrupted by longer pauses. Ausculation, after having spanked the child a few times, reveals crepitant riles usually over the bases (atelectatic crepi tations). In some children one observes localized lateral retractions,
also at times in the middle of the sternum. Now and then severer at tacks of cyanosis intervene without warning. With a falling tempera ture and marked loss of weight, the children die usually within a few days and often even within a few hours. Now and then the asphyxia occurs, especially in premature children, as late as a few weeks after birth and is then usually a very bad sign.
The pathological anatomical findings are often totally negative except for a more or less extensive pulmonary ateleetasis.
The diagnosis is furnished by the pulmonary findings, the impair ment of respiration, the increasing stupor and the poor appetite.
The prognosis depends, first, on the cause underlying the asphyxia. It depends further on the treatment instituted. Should any improve ment of the condition be secured by means of the therapeutic measures, one usually wins the battle. This, however, does not hold good for the cases of asphyxia occurring later in premature children, which usually terminate fatally.
The treatment of acquired asphyxia consists chiefly in the use of hydrotherapeutic measures. The alternating hot and cold baths recom mended, under 2, for congenital asphyxia, often prove valuable when frequently repeated. Heubner recommends baths at 35° C. (95° F.) of only short duration, combined with pouring cold water 10-12° C. (50-53 ° F.) over the chest, back and head four to six times, using one pint each time and repeating regularly every two hours. Besides this, warmth and breast-feeding. In these cases oxygen inhalations are espe cially recommended. The other therapeutic measures recommended for congenital asphyxia may also be symptomatically employed.