VI. EFFECTS OF DEFICIENCY 239 



rounded character of the rib angle. Most important of all is what happens 

 at the costochondral junction. Normally, the cartilage and rib shaft are 

 accurately and rigidly joined end to end. In rickets, they are separated by 

 the soft metaphysis, which has little or no rigidity and permits of consider- 

 able movement chu'ing respiration. The metaphysis soon gives way to the 

 negative intrathoracic pressure, the ribs become more and more bent in- 

 ward, until finally the rib ends lie internal to the cartilage, and the enlarge- 

 ment of the costochondral junction is within the chest and compresses the 

 adjacent lung. Thus the lung is divided into an anterior emphysematous 

 portion and a posterior portion which is partlj^ emphysematous and partly 

 atelectatic separated by a longitudinal zone of complete atelectasis. 



As one watches such a child breathe, he observes that with inspiration 

 almost every one of these deformities becomes exaggerated. The moment 

 inspiration ends, the chest in early cases springs into the expiratory posi- 

 tion. Observation, or measurement, will reveal that the inspiration has 

 barely, if at all, increased the chest circumference. Moreover, it appears 

 that life is maintained not by the awkward and inefficient movement of 

 the rib cage, but by the exertions of the diaphragm. Later the elasticity of 

 the thoracic cage is lost and even the diaphragm is partly relaxed during 

 rest. 



The essential difficulty physiologically is the loss of thoracic rigidity. As 

 this process progresses, the linear depressions which at first were present 

 only during inspiration tend to persist in expiration. As the efficiency of 

 each respiration is diminished by the chest collapse and the intrusion of 

 costochondral junctions and the rib ends into the chest cavity, there is an 

 attempt at compensation by increasing the freciuency of respiration. But 

 the greater and more frecjuent the force applied, the greater is the collapse. 

 The diaphragm pulls its attachments further inward, and the accessory 

 muscles of respiration draw the bones out of position without stabilizing 

 the chest as a whole. As there is progressive decrease in chest capacity, 

 there develops increasing atelectasis, the pressure in thepulmonary circula- 

 tion rises, the right heart hypertrophies, and cyanosis may appear. The 

 dyspnoea is extreme, the respirations rising to 60 and 100 times a minute. 

 There may also appear dilatation of the nostrils, a grunt and a cough. If, 

 now, an additional burden, such as an infection, is superimposed, the mech- 

 anism and its compensations may fail, the vital capacity becomes ecjual to 

 or less than the tidal air, and permanent cyanosis is the I'esult. Sudden 

 death may follow. 



On the other hand, if the child does not die, he may improve. As the 

 rickets heals and lime salts are deposited in the bone, the chest regains its 

 rigidity. Despite the persistence of deformities, the efficiency of respiration 

 improves and then may gradually return to normal. 



In neo-natal rickets, the pelvis becomes flattened, by virtue of the pull 



