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Mabel Sutter, D. 0.



CALIFORNIA COLLEGE OF MEDICINE




PEDIATRICS



The Hygienic and Medical Treatment



OF



CHILDREN



BY

CHARLES HUNTER DUNN, M. D.

INSTRUCTOR IN PEDIATRICS, HARVARD UNIVERSITY
PHYSICIAN IN CHIEF AT THE INFANTS' HOSPITAL



FOUNDED UPON THE TEACHINGS OF THOMAS MORGAN ROTCH, M. D.



VOLUME II
Third Edition



THE SOUTHWORTH COMPANY, PUBLISHERS

TROY, NEW YORK

1922



100



COPYRIGHT 1917-1920-1922
BY THE SOUTH WORTH COMPANY



<3fart rngc ^Jrres
THE BRANDOW PRINTING Co.

ALBANY, N. Y.



To

CLARENCE JOHN BLAKE, M.D., O.M. (Vienna), F.A.C.S.

Professor of Otology (Emeritus), Harvard University

THIS VOLUME is INSCRIBED

As a tribute to his high professional attainments and to his unfailing

interest in the welfare of children, and in grateful

remembrance of many acts of kindness

BY THE AUTHOR



>



CONTENTS

DIVISION VI

DISEASES DUE TO DISTURBANCES OF METABOLISM OR TO

CONSTITUTIONAL ANOMALIES PAGE

Rachitis 2

Scorbutus 28

Purpura 41

Hemophilia 51

Acidosis 54

a. Cyclic Vomiting 59

b. Acid Intoxication 61

Diabetes Mellitus 73

Diabetes Insipidus 79

Spasmophilia 82

Pellagra 97

DIVISION VII

Till: SPECIFIC INFECTIONS

Scarlet Fever in

Measles ._ 135

Rubella 151

Dukes' Disease 155

Varicella 157

Variola 164

Vaccinia 171

Diphtheria 176

Pertussis 214

Mumps 231

Influenza 237

Typhoid Fever 244

Malaria 260

Epidemic Cerebrospinal Meningitis 273

Poliomyeloencephalitis 295

Rheumatic Fever 319

Erysipelas 339

Tuberculosis 345

Syphilis 389

DIVISION VIII

DISEASES OF THE LARYNX, LUNGS AND PLEURA

I. DISEASES OF THE LARYNX 422

Acute Laryngitis 423

Edema of the Larynx 429

Congenital Laryngeal Stridor 430



vi CONTENTS

I. DISEASES OF THE LARYNX Continued PAGE

Foreign Bodies in the Larynx 431

Papilloma of the Larynx . 432

Chronic Laryngitis 433

II. DISEASES OF THE LUNGS 434

Acute Bronchitis 434

Fibrinous Bronchitis 44 2

Chronic Bronchitis 442

Bronchopneumonia 444

a. Secondary Bronchopneumonia 446

b. Tuberculous Bronchopneumonia 460

c. Influenza Bronchopneumonia 467

d. Primary Pneumococcus Bronchopneumonia 470

e. Terminal Bronchopneumonia 471

f . Friedlander's Pneumonia 471

Lobar Pneumonia 472

Hypostatic Pneumonia 497

Gangrene arid Abscess of the Lung 497

Atelectasis 498

Emphysema 498

Bronchiectasis 498

Asthma 500

III. PLEURISY 508

Empyema 508

Serous Pleurisy 5 20

Fibrinous Pleurisy 525

Chronic Adhesive Pleurisy '. . . . 527

LIST OF ILLUSTRATIONS

PLATE COLORED PLATES PACK

III. Infantile Scorbutus 29

VIII. Scarlet Fever and Measles 118

IX. Koplik's Spots 138

X. Vaccination 1 74

XI. Varicella, Syphilis, and Erysipelas 158

XII. Diphtheria 182

154. Facial Erysipelas 339

FIG. FULL PAGE ILLUSTRATIONS PAGE

118. Rachitis, age six years 17

182. Improvised crib tent for steam inhalations 427

185. Secondary bronchopneumonia 451

186. Secondary bronchopneumonia 453

188. Secondary bronchopneumonia; roentgenogram 455

189. Secondary bronchopneumonia; roentgenogram 455

190. Bronchopneumonia; roentgenogram 455

191. Tuberculous bronchopneumonia, subacute type 463

192. Tuberculous bronchopneumonia; roentgenograrn 464

193. Tuberculous bronchopneumonia; roentgenogram 465

194. Tuberculous bronchopneumonia; roentgenogram 466

201. Lobar pneumonia; middle lobe 483

202. Lobar pneumonia; roentgenogram 486



CONTENTS vii

203. Lobar pneumonia; roentgenogram 488

209. Empyema, small effusion 515

210. Empyema; roentgenogram 516

211. Empyema; roentgenogram 517

212. Empyema with pneumo thorax; roentgenogram 519



FIG. ILLUSTRATIONS IN THE TEXT PACE

109. Rachitic bone 3

no. Spindle-shaped rachitic bone. 4

i ii. Rachitis with enlarged spleen 5

] 1 2 The rachitic head 1 1

1 1 3. Rachitic rcsc ry 13

1 14. Position of the rachitic rosary 14

115. Rachitic kyphods 14

116. Rachitic deformity of the spine and chest 15

117. Rickets , 16

119. Rickets with deformity of the humeri 17

1 20. Roentgenogram of rickets 19

121. Section of scorbutic bone 31

122. Infantile scorbutus in an infant of nine months 33

123. Infantile scorbutus 34

124. Scorbutus; roentgenogram 35

125. Scorbutus; roentgenogram 36

126. Scorbutus; roentgenogram 36

127. Scorbutus; roentgenogram 37

1 28. Tetany 87

129. Pellagra '. 101

130. Pellagra ' ' 102

131. Pellagra in Italy 103

132. Pellagra 104

133. Pellagra in Italy 105

134. Varicella, third day 159

135. Apparatus for intubation 206

136. Intubation; beginning of the insertion of the tube 207

137. Intubation; completing the insertion of the tube 208

138. Intubation; withdrawing the tube 210

139. Pertussis during the paroyxsm 219

140. Submaxillary mumps 234

141. Influenza bacilli in the sputum 239

142. Typhoidal ileo-colitis 246

143. Malaria with enlarged spken 267

144. Malaria with enlarged spleen 268

145. .Opisthotonos in meningitis 277

146. Chronic meningitis 278

147. Injection of serum into the spinal canal 286

148. Tapping the cerebral ventricles 289

149. Injection of serum into the cerebral ventricles 290

150. Position of insertion of the needle in tapping the cerebral ventricles 291

151. Poliomyeloencephalitis 303

152. Poliomyeloencephalitis : 313

153. Rheumatic fever 326

155. Tuberculcsis; primary lesion in the lungs 352

156. Tuberculosis; primary lesion in the lungs 353



viii CONTENTS

FIG. PAGE

157. Miliary tuberculosis of the lungs 358

158. Miliary tuberculosis of the lungs 359

159. Tuberculous bronchopneumonia 360

1 60. Tuberculous bronchopneumonia 361

161. Tuberculous bronchopneumonia 362

162. Tuberculous ulcer of the secum 363

163. Tuberculous ulcers of the intestine 364

164. Tuberculous ulceration of the intestine 365

165. Tuberculous meningitis 366

166. Tuberculous dactylitis 369

167. Tuberculous dactylitis 370

168. Examination for d'Espine's sign 372

169. Chronic tuberculosis 373

170. Tuberculous ; primary stage 380

171. Tuberculous; primary stage 381

172. Tuberculosis bronchopneumonia 382

173. Syphilitic maculae, ulcers, arid bullae 399

174. Syphilitic osteochondritis 4<^o

175. Syphilitic dactylitis 401

1 76. Late manifestations of syphilis 404

177. Syphilitic periostitis 405

178. Syphilitic periostitis 406

179. Hutchinson's teeth 407

1 80. Technic of injecting neosalvarsan 417

181. Congenital syphilis 419

183. Lesion of secondary bronchopneumonia 448

184. Lesion of secondary bronchopneumonia '. 449

187. Acute bronchopneumonia 454

195. Lobar pneumonia 480

196. Lobar pneumonia 481

197. Lobar pneumonia; upper lobe in front 482

198. Lobar pneumonia; upper lobe behind 482

199. Lobar pneumonia; lower lobe in front 483

200. Lobar pneumonia; lower lobe behind 483

204. Bronchiectasis 499

205. Empyema from in front 513

206. Empyema from behind 513

207. Empyema, large effusion, front 514

208. Empyema, large effusion, from behind 514



DIVISION VI

DISEASES DUE TO DISTURBANCES OF
METABOLISM OR TO CONSTITU-
TIONAL ANOMALIES

In this division are grouped a number of diseases of which the
etiology is not definitely known. They are probably due to various
abnormalities of the chemistry of the body, and consequently might
be defined as constitutional diseases. The most probable cause of
chemical abnormality is disturbance of metabolism, and this is the
probable pathogenesis of the majority of the diseases of the group
described in this division. In the case of hemophilia, however, the
probability is that the disease is due to the direct inheritance of a
constitutional abnormality, which involves the chemistry or struc-
ture of certain of the body tissues. In the other conditions, the
cause of the chemical abnormality being unknown, it is attributed
to disturbed metabolism. Whether or not an inherited constitu-
tional abnormality plays a part, and if so, to what extent, and
whether or not the chief part is played by causes acting from out-
side the body, and if so, to what extent, are unknown. Whatever
the cause, these diseases present manifestations which strongly sug-
gest that the tissue lesions, or functional disturbances produced, are
due to disturbed metabolism.

Abnormality of metabolism produces two kinds of effects. The
first effect is disturbance of nutrition. This may affect the body
as a whole, or may affect certain particular tissues of the body. The
result of disturbance of nutrition in childhood is an abnormality of
development, with characteristic tissue lesions. The most conspic-
uous example of this effect of disturbed metabolism is the disease
rachitis.

A second effect of an abnormality of metabolism is the formation
of toxic products, resulting in a toxemia. The results of toxemia
are again two-fold, one being the production of definite tissue lesions
from the action of the poison, as in purpura, while the other result
is a disturbance of function, as seen in spasmophilia.

The following scheme illustrates the probable pathogenesis of the
diseases of this group:



CONSTITUTIONAL DISEASES

(Lesions



Constitutional Abnormality



Unknown Causes from Outside Body



Disturbances j

of Functional

.Nutrition [Disturbance
Disturbances

of
Metabolism

Lesions



Toxemia



Functional
Disturbance



RACHITIS

(Rickets)

Rachitis, or rickets, is a constitutional disease, with definite ana-
tomical lesions, which certainly represent a disturbance of nutrition.
This in turn is almost certainly due to a disturbance of metabolism.
All the organs and tissues are involved to some extent in the nutri-
tional disturbance, but the principal lesions are in the bones. The
nutritional disturbance produces the characteristic skeletal lesions
by affecting the anatomical growth and development of the osseous
tissue. As the lesions are the central feature of the disease, and
as a knowledge of the tissue changes are essential to an understand-
ing of the theories of the etiology of the disease, the pathological
anatomy and chemistry of rickets will be described first.

PATHOLOGICAL ANATOMY. BONE LESIONS The patholog-
ical lesions of rachitis are represented chiefly in the bones, and occur
during the period in which the normal processes of ossification are
most active, that is, during the first year and the first part of the
second year of life.

The normal growth of bone depends upon four conditions : (a) mul-
tiplication of cartilaginous cells in definite lines, followed by (b) cal-
cification of the intercellular spaces; (c) the formation of medullary
spaces by the penetration of the blood vessels, with subsequent
absorption of tissue; and (d) finally, the concentric deposition of
calcium within the medullary spaces. The bones grow in length by
the production of bone-tissue in the cartilage between the epiphysis
and the diaphysis, and in thickness by the growth of bone from the
inner layers of the periosteum. At the same time the medullary
canal is enlarged in proportion to the growth of the bone by the
absorption of its inner layer. These processes progress in definite
order and in clearly defined zones.

In rachitis the chief microscopic features are the changes which
occur in the zones of growth and the asymmetrical character of the
proliferative processes. The cartilaginous and sub-periosteal cell-
growth which produces ossification goes on with increased rapidity
and in an irregular manner both between the epiphysis and the dia-



RACHITIS



physis and beneath the periosteum. If we examine microscopically
the region between the epiphysis and the diaphysis, usually called
the zone of proliferation, we find that the cartilaginous cells are not
regularly arranged in rows around a definite zone in advance of the
ring of ossification, as in normal tissue, but there is an irregular
heaping up of cartilaginous cells, sometimes in rows, sometimes not,
covering an ill-defined irregular area. This zone of proliferation also,
instead of being narrow and sharply defined, is quite lacking in uni-
formity. It presents a broad, reddish-gray appearance, with marked
thickening and hyperemia. The medullary spaces are much more
vascular than normal, and are so increased in area as to extend into




-Z.P.




I. Normal bone: Z. P., zone of proliferation. II. Bone of a cretin: Z. P., zone
of proliferation. III. Rachitic bone: Z. P., zone of proliferation

the zone of calcification, and sometimes through it. The deposit
of calcium within these spaces is, however, either absent or very
irregular, and is for the most part replaced by a soft, friable sub-
stance, consisting of a bone-tissue that is very lacking in lime-salts,
with cells of various kinds embedded in a fibrillated ground-substance.
This tissue is called "osteoid," and is similar to that formed by
osteoblasts.

In the region of ossification (ends of diaphysis and epiphysis)
there is microscopically a pronounced increase of blood-vessels and
cartilage-cells, with lengthening of cell columns, and disturbance of
calcification of the intercellular substance. Calcification, if present,
may be isolated in the region of the proliferating cartilaginous cells,



4 CONSTITUTIONAL DISEASES

or may be altogether absent over considerable areas. The sub-
periosteal layer of cells, which is normally thin and scarcely notice-
able microscopically, becomes hyperemic and thickened, with an
appearance similar to that of spleen-pulp. Beneath this perio-
steum is also to be found the "osteoid" tissue seen in the zones
of proliferation.

The medulla of the bone is more hyperemic even than normal.
Its tissue is rich in cells, and like the fetal medulla, contains dilated

FIG. no




Spindle-shaped rachitic bone



vessels and fat. The intercellular substance may show mucoid
degeneration or even be of fluid consistency. In such a condition
it does not seem that lime is dissolved from the bone tissue by the
blood, but it is the resorption of such bone in toto that is the im-
portant factor in the process. Resorption at the age at which ra-
chitis occurs is normal. In rickets, rapid cases of softening certainly



RACHITIS 5

show increased resorption. Ordinarily, with a resorption not greatly
increased, the formation of fresh bone containing but little lime
results in loss of strength. In the skull, in some places, absorption
predominates (occiput); in other cases accretion of osteoid tissues
(frontal and parietal eminences). Deficient bone-growth is the
simple cause of enlarged fontanelles. In convalescence, lime is de-
posited in the previous limeless osteoid tissue, and the result is a
thick and heavy bone. In fractures at this period callus-formation
is intense and excessive.

The excessive proliferation of cells in the inner layers of the peri-
osteum, the irregular calcification which occurs about them, and the
absence of uniformity in the elaboration of the structure of the
bone, produce an irregular, spongy bone-tissue instead of the com-
pact lamellated tissue which is so necessary for the uniformity of
the structure. The increased cell-growth between the epiphysis and
the diaphysis produces the peculiar knobby swellings which are
characteristic of rachitis. At the same time the medullary cavity

FIG. in




Male, 3 years old. Rachitis, with enlarged spleen

increases rapidly in size, and the inner layers of the bone become
spongy. The result of these processes is to diminish the solidity
of the bones so that they cannot resist the strain of the muscles or
outside pressure, and consequently become bent and curved. After
a time the rachitic process may stop and the bones may assume a
more normal character. The porous bone-tissue becomes compact,
and even unnaturally dense, so that in later childhood the rachitic
bone is unusually hard, like ivory, a condition noticed by those who
have to operate on these bones.

VISCERAL LESIONS; SPLEEN. Investigations have shown that in
cases of rachitis which come to autopsy, the spleen is invariably en-
larged, with the exception of the cases of clearly pronounced atrophy,
in which the spleen is of normal size and weight or below normal. A



6 CONSTITUTIONAL DISEASES

second marked characteristic is the more or less significant thicken-
ing of the capsule and the increase in the consistency of the organ.
The third peculiarity of the rachitic spleen is the anemia of the organ
and the diminution in the number of Malpighian bodies, which in
children are otherwise well developed, but in these conditions are
hardly perceptible. On section, the spleen has a blood-red color, the
trabeculae are clearly marked by interlacing threads, and on draw-
ing the knife over the cut surface there remains upon the edge blood
and pulp tissue. The characteristics described hold true in all cases
of rachitis, and, in general, indicate approximately the intensity of
the changes in the bones.

The microscopic appearances are those of an interstitial splenitis.
Whether the inflammatory appearances are directly dependent upon
the rachitis or are due to the complicating diseases which caused
the death of the patient has never been definitely determined. The
uniform appearances in all the cases irrespective of the cause of
death, seem to give weight to the opinion that the lesions are directly
connected with rachitis.

PATHOLOGICAL CHEMISTRY. The rachitic bone and carti-
lage is abnormally poor in mineral constituents, that is to say, in
calcium and phosphorus. The ash content of the ribs and spine
may be reduced to from sixty to twenty per cent of the normal.
Metabolism experiments up to the present time have only succeeded
in establishing the fact that the diminished calcium content of the
skeleton in rachitis is due to diminished calcium retention a nega-
tive calcium balance, and that in the healing stage the calcium bal-
ance is reversed. This is no more than would be expected from
the character of the condition. Up to the present time, metabolism
experiments have been unable to throw further light on the path-
ological chemistry of rachitis.

-ETIOLOGY. THE NATURE OF THE DISEASE. The cause of
rachitis is unknown. The disease is almost certainly a disturbance
of nutrition, and the bony lesions being the most prominent feature
of the disease, it has been assumed by many writers that rachitis
represents a disturbance of the calcium metabolism. That the cal-
cium balance is disturbed in rachitis is an undoubted fact, but this
does not mean that the disturbance of calcium metabolism is the
primary factor in the etiology of the disease. That rachitis is due to
insufficient calcium in the food, or to insufficient absorption of cal-
cium from the intestine, has never been proven, and is certainly
contrary to the evidence. There remains the possibility that the
disturbance involves the utilization of calcium by the tissues of the
body. Sufficient calcium is absorbed, but not being used, is excreted
again into the intestine. Under this theory, inability to use calcium



RACHITIS 7

leads to the formation of lime-poor bone, which interferes with endo-
chrondral ossification. The other characteristics of the osseous lesions
are considered secondary to this, the new cartilage being irregularly
formed, while the medullary spaces, and an excessive number of
blood vessels, project into the defective cartilage.

Another possibility is that the formation of defective bone tissue
precedes and is the cause of the abnormality of the calcium meta-
bolism. If this is the case, some other cause must be sought for the
osseous lesions. The choice between these two theories must be a
matter of opinion. I believe the weight of evidence to be against
the theory that a specific disturbance of calcium metabolism is the
primary factor. I believe that the calcium metabolism is disturbed
only in this one respect, that the bony tissue is so affected by the
disease that it is unable to seize and utilize the lime salts which are
abundantly present for its use.

This does not, however, explain why the bony tissue is unable
to utilize the lime salts. One theory, advanced by some writers, is
that there is a special pathological peculiarity of the bony tissue
which prevents ossification in rickets. Against this is the fact that
rickets is not a disease limited to the bones, but affects all the organs
and tissues of the body, which suffer in a manner which suggests
disturbance of nutrition. If the bony tissues suffer with them, as
a result of such disturbance, the effect in growing bone would quite
naturally manifest itself by inability to carry on the most important
function of such tissue, which is the storing of calcium. Moreover,
histological and microchemical researches have given no evidence
of any primary anatomical peculiarities of the bony tissue of the
rachitic child, the lesions being suggestive of impaired nutrition.

The theory that a disturbance of metabolism in rickets causes an
increased quantity of acid in the circulating body fluids, and that
decalcification occurs through their influence, has not been supported,
and is contrary to the preponderance of the evidence at hand.

From present knowledge, it can only be concluded that the disease
rachitis represents a general disturbance of nutrition, in which all
the tissues of the body suffer to some extent. Among them the
bony tissue suffers, and the disturbance of nutrition so affects the
growing bone, as to produce the characteristic osseous lesions of the
disease. The effect of these lesions is impaired power of utilizing
lime salts, and this leads to diminished calcium retention.

THEORIES AS TO ETIOLOGY. In the voluminous literature of
rickets will be found four principal theories as to the etiology of the
disease. These are that the disease is caused, first, by an infec-
tion, second, by a disturbance of function of some of the ductless
glands, third, by an unsuitable diet, and fourth, by bad hygienic
surroundings.



8 CONSTITUTIONAL DISEASES

The evidence in favor of the infectious nature of rachitis is very
slight, and inconclusive. The weight of evidence points toward
disturbance of metabolism as the most probable cause of the im-
paired nutrition.

The recent attempts to prove that some of the disturbances of
metabolism are due to an impairment of the function of some of the
ductless glands, such as the thyroid, parathyroid, thymus, and adre-
nals, have not been successful.

The two principal theories of the etiology of rachitis are the dietary,
and the hygienic. According to the former, the disturbance of meta-
bolism in rickets is caused by an improper diet. In favor of this
theory are the facts that rickets is commoner in artificially-fed infants
than in the breast-fed, and that it is also commoner when artificial
feeding is badly conducted than when it is rationally conducted.
Against it is the fact that the occurrence of rickets has never been
conclusively associated with any particular dietary error, nor with
any particular form of gastro-intestinal disturbance. Indeed, rickets
is comparatively uncommon in the well-known gastro-intestinal
diseases which lead to interference with growth, and atrophic infants
are very infrequently severely rachitic. It is often seen hi fat chil-
dren, who have never had any digestive disturbance, and indeed,
the disturbances of digestion in rickets seem to be usually secondary
to the disease. The occurrence of rickets in fat children might partly
be explained by diminution in their bodily activity.

It was formerly supposed that the most probable error in diet
responsible for rickets was insufficient fat in the food. This was
based on the statistical evidence obtained from the study of the
previous diet of rachitic patients. The majority had been fed on
foods high in carbohydrate, and low in fat, such as the various pro-
prietary infant-foods. Such foods, however, are most commonly in
use among the poorer members of society, where children are sub-
jected to the worst errors of hygiene. Consequently no positive con-
clusion as to the influence of diet can be drawn from such statistics.

Metabolism studies on the effects of fat and carbohydrate on
calcium metabolism, have suggested just the reverse theory as to
the dietary error which causes rachitis. It has been shown that
overfeeding with fat causes a negative calcium balance, while car-
bohydrate favors calcium retention. This phenomenon would only
be of value in the etiology of rachitis, if the theory that the disease
is due to a negative calcium balance were proven. It is possible,
however, that overfeeding with fat may be a contributing cause.

No influence of diet on rachitis has yet been conclusively proven



Online LibraryCharles Hunter DunnPediatrics, the hygienic and medical treatment of children (Volume 2) → online text (page 1 of 55)