chapter entitled "Secondary Diphtheria." In it the author says, what
all who are familiar with diphtheria will agree to, that secondary
diphtheria does not differ in nature from the primary form, and that
it exhibits a tendency "to occupy the organs which are themselves the
seat of the more pronounced local determinations of the primitive
malady.... Diphtheria is seen in the course or sequel of numerous
diseases. Some appear to have a special proclivity for engendering
diphtheria; these are specific maladies: measles, scarlet fever,
pertussis." I have tabulated as follows Sanné's statistics of
secondary diphtheria:
Cases Deaths Cures Doubtful
----- ------ ----- --------
Diphtheria complicating measles, 100 83 15 2
" " scarlet fever, 43 22 17 4
" " pertussis, 20 12 6 2
" " typhoid fever, 8 8
" " tuberculosis, 19 19
Sanné's statistics relating to the seat of scarlatinous diphtheria are
as follows:
Fauces alone attacked, 15 cases.
" with larynx " 4 "
" " nasal fossa " 8 "
" " larynx and nasal fossa " 4 "
" " larynx and bronchi " 1 "
" " nasal fossa and lips " 1 "
" " lips and skin " 1 "
" unaffected, 3 "
Diphtheria generalized, 2 "
Larynx only affected, 2 "
Nasal fossa " 1 "
The opinion of so good an observer as Sanné, that when in scarlet
fever, pseudo-membranous exudation appears upon the mucous surfaces
which are the seat of scarlatinous inflammation, diphtheria has
supervened, and not a croupous form of scarlatinous phlegmasia,
carries with it great {516} weight. That it was diphtheria in four
instances in my practice I had sufficient proof, for this disease
became dissociated from scarlet fever, and extended to other members
of these families as idiopathic diphtheria.
Nevertheless, one of the most difficult problems which we have to deal
with in certain cases is to distinguish diphtheritic from
non-diphtheritic inflammation; and I see no reason why the
scarlatinous inflammation when intense may not be sometimes
membranous; and those no doubt err who ignore this, and consider every
inflammation attended by a pellicular exudation diphtheritic. We know
that in some cases of dysentery a fibrinous exudation occurs upon the
surface of the colon; that in croupous pneumonia fibrin exudes into
the bronchioles and alveoli of the lungs; and that physicians in
localities where there is no diphtheria meet, though at long
intervals, cases which they designate croupous pharyngitis and
laryngitis; and it seems to me that the intense inflammation of
anginose scarlatina probably sometimes produces the same exudation.
Moreover, it is very difficult to distinguish in the swollen fauces
between a membranous exudation and ulceration or superficial gangrene
so common in malignant scarlet fever. The grayish-white surface,
jagged and foul, may be the one or the other, an exudation or a
sphacelus, and in certain instances it is impossible to discriminate
between the two conditions at the bedside.
Diphtheria complicating scarlet fever sometimes begins nearly
simultaneously with the latter. Henoch states that exceptionally he
has observed suspicious patches upon the fauces before the appearance
of the scarlatinous eruption upon the skin; and he adds: "I have had
repeated opportunities of observing this unusual beginning. In such
cases we must ask ourselves whether the first affection was really
connected with the second, or whether the former was a true primary
diphtheria, rapidly followed by scarlatina. This opinion is favored by
the fact that I have only observed such cases in the hospital, in
which infection with various forms of contagion can scarcely be
avoided."
But usually it is not till the third or fourth day of scarlet fever
that this complication begins. The patient has been progressing
favorably with the scarlet fever, till on a certain day a marked
aggravation of symptoms occurs. A higher temperature, more pungent
heat, and the physiognomy of a more serious malady are present. On
inspecting the fauces to discover the cause we observe a pellicle
forming over the tonsils and perhaps other portions of the faucial
surface. Often the entire aspect of the case changes by the occurrence
of this complication, a mild case of scarlet fever becoming grave and
fatal in consequence. Thus in a case which I saw with Dr. Hardy of New
York the membranous inflammation of diphtheria, commencing upon the
fauces on the third day of scarlet fever, extended to the Schneiderian
membrane, and thence along the left lachrymal sac to the eyelids,
producing redness and swelling along the side of the nose and upon the
cheek like that of erysipelas. A thick diphtheritic pellicle occurred
upon the under surface of each eyelid on the left side, with great
tumefaction of both lids, gangrene of the cornea, and destruction of
the eye. The case soon ended fatally.
The diphtheritic inflammation sometimes extends to the larynx and
trachea, producing hoarseness and more or less obstruction to {517}
respiration. A thin film or flakes of fibrinous exudation, rendering
the respiration noisy, developed on the laryngeal or tracheal surface,
is, I think, not infrequent in diphtheria complicating scarlet fever,
but the rapid development of a thick and firm pseudo-membrane, so as
to imperil the life of the patient from the stenosis in the
air-passages, has been much less frequent in my practice than it is in
primary diphtheria and in diphtheria complicating measles or
pertussis. The following were cases of this severe complication
occurring in a recent epidemic in the New York Foundling Asylum. In
these cases the respiration was noisy, but the obstruction to
breathing seemed to be due to infiltration and swelling around the
aperture of the glottis, rather than to diphtheritic croup, which the
autopsies showed to be present.
_Case 2._--A child aged three and a half years, who previously had
symptoms of mild catarrhal croup, with moderate redness of the fauces,
sickened with scarlet fever on Oct. 1, 1882, the rash being profuse
and soon covering nearly the entire body. The axillary temperature was
103°, pulse 140; slight stridor in breathing and some cough; fauces
very red, but free from membrane. Oct. 2d, restless, sleeping but
little; has vomited four times. Oct. 3d, temp. 103.5°, pulse 120;
fauces much swollen; still vomiting; rash abundant. 4 P.M., temp.
104.3°, pulse 128; tongue clean; some discharge from nares; urine not
albuminous, but its quantity diminished. Oct. 4th, aspect that of very
severe sickness; profuse discharge from nostrils; fauces of a deep red
color, and a diphtheritic pellicle over tonsils and uvula; tumefaction
along the sides of the neck; temp. 104°, pulse 140; breathing
moderately stridulous; urine is passed more freely than yesterday;
evening temp. 105°. Oct. 6th, croupy symptoms more marked; tonsils and
uvula greatly swollen, so that the fauces are almost occluded; temp.
103.5°; breathing difficult, but apparently sufficient oxygen is
received; profuse nasal discharge, and other symptoms as before. About
1.30 P.M. he was raised to take some milk, and suddenly became
asphyxiated. His face was dusky, his eyes protruded, and he voided
urine and feces. Dr. Swift, who attended the child, and to whom I am
indebted for this history, immediately performed tracheotomy, which
gave temporary relief by the expulsion of a considerable quantity of
pseudo-membrane through the opening. On the following day the
respiration again became obstructed at some point below the canula, so
that it could not be removed; the features grew livid, and death
occurred in convulsions twenty-six hours after the tracheotomy.
The autopsy was made by Dr. W. P. Northrup, curator of the asylum, who
found the pharynx covered by a membrane which was traced to the
posterior nares; larynx, trachea, and bronchial tubes as far as the
third divisions also covered with membrane; portions of the tracheal
surface denuded, and the mucous membrane underneath of a bright red
color and smooth; tonsils sloughy and fetid; mucous membrane of
smaller bronchial tubes very red and covered with viscid mucus and
pus; a portion of the left lung, extending from the root posteriorly
to the surface, gangrenous, discolored, and honeycombed; two or three
intensely hyperæmic spots, as large as a bean, in left lung; right
lung congested, but not consolidated; slight catarrh of stomach;
circumscribed areas of congestion in intestines; solitary glands of
intestines swollen, and some {518} of them ulcerated; spleen of normal
size, rather pale; liver congested and somewhat enlarged.
_Case 3._--Katie, aged six and a third years, was returned to the
asylum on Nov. 18th. Three days later (Nov. 21st) she had sore throat,
reddened fauces, coated tongue, and a faint rash upon the neck, chest,
and arms; eyes injected; temperature 102°. In the afternoon
temperature 103°; eruption still faint. Nov. 22d, temperature 103.5°;
an eruption on chest, abdomen, arms, and legs in patches. Evening,
temperature 104°; voice clear. Nov. 23d, temperature 103.5°; tongue
red; fauces deeply reddened, but without any visible pseudo-membrane;
eruption of a scarlatinous appearance over the back and abdomen; on
the extremities dusky, livid patches. P.M., temperature 104°; is
slightly delirious; eruption abundant. Nov. 24th, temperature 103.5°;
eruption well out on abdomen; it is the same as yesterday upon the
extremities, except perhaps a little more dusky; still no
pseudo-membrane to be seen upon the fauces; is restless and delirious.
P.M., during the day has been very restless, suffering from dyspnoea;
no croupy voice nor croupy cough, though the dyspnoea continues, and a
pseudo-membrane is now visible over the tonsils and adjacent faucial
surface; eruption dusky; skin cool; pulse very frequent and feeble.
From this time she sank steadily, and died at 11.30 P.M. During her
sickness her urine seemed to be diminished, but it was not properly
examined.
Autopsy Nov. 25th by Dr. W. P. Northrup, curator: Points of redness,
apparently a hemorrhagic eruption, over the face, shoulders, and parts
of the trunk; a few of the same on the extremities; no pseudo-membrane
visible in nostrils or in buccal cavity; brain not examined.
Naso-pharynx covered by a thick fibro-purulent membrane. Larynx
contains a well-marked pseudo-membrane, but not continuous. Trachea
covered by a pseudo-membrane, continuous over most of its surface, but
in places broken and flaky. Where it is detached the mucous membrane
is seen underneath, dusky and deeply injected. At the root of the
lungs the pseudo-membrane can be traced along the tubes about an inch
in all directions. Lungs oedematous, with deep congestion in places,
but apparently no pneumonia; about two drachms of clear, straw-colored
fluid in pericardium; a few stringy decolorized clots in the cavities
of the heart; left ventricle contracted. The heart-fibres, carefully
examined, microscopically, in the laboratory, are found to be normal,
not having undergone granular or fatty degeneration. Liver normal in
size; pale-yellow areas upon the superior surface, either from anæmia
or fatty deposition. Kidneys of usual size, capsule not adherent;
pyramids congested; cortex pale; markings distinct. Spleen enlarged
about one-third; consistence normal. Stomach and intestines not
examined.
_Case 4._--Scarlet fever complicated by diphtheria, nephritis, and
broncho-pneumonia. (History by house physician, Dr. Swift.) Phoebe,
aged three and a quarter years, was delicate, but in her usual health
till Oct. 29, 1882, when she became languid and vomited several times,
and her tongue was coated. Oct. 30th, occasional vomiting; fauces
reddened; tongue coated. Oct. 31st, remains languid; fauces deeply
reddened; a faint scarlatinous eruption over back, wrists, and feet;
temperature 100.5°. P.M., eruption of scarlet fever well out over the
surface; tongue cleaner. Nov. 1st, {519} rash over entire body;
temperature 100.2°. Nov. 2d, fauces deep-red; tonsils and uvula
swollen; diarrhoea and vomiting. Nov. 3d, temperature 102.5°; the
eruption, which has been bright red, is now more dusky. Nov. 5th,
temperature 104.5°; dusky-red color of the eruption; skin beginning to
desquamate in places; urine normal; a discharge from nostrils. Nov.
6th, temperature 103.5°; eruption still present, but skin of abdomen
and back desquamating; has otorrhoea on both sides; fauces deeply
hyperæmic, but no pseudo-membrane visible upon them. Nov. 7th,
temperature 103°; respiration and cough have a slight croupy
character; other symptoms as yesterday. Nov. 8th, temperature 101°. A
careful inspection of the fauces shows that it contains no
pseudo-membrane; nostrils discharging a dark-brownish liquid;
examination of urine negative. Nov. 11th, eruption, which appears to
have been hemorrhagic in points, is fading and the desquamation is
less. Nov. 14th, nostrils still discharging; glands of neck swollen.
Nov. 16th, temperature 103°; sp. gr. of urine 1010, no casts, nor
albumen; the chest seems clear; less discharge from nostrils; fauces
clean and but slightly inflamed. Nov. 17th, 18th, temperature 103.5°;
vomits; lungs healthy, but breathes with considerable effort, though
without stridor; urine diminished; its sp. gr. 1020, albuminous,
contains blood-corpuscles and granular casts. Nov. 19th, is very
pallid; temperature 104°; very restless; vomits; urine diminished;
bowels freely open. Nov. 20th, respiration still embarrassed;
subcrepitant râles over the entire chest and percussion resonance not
clear; temperature 102.5°. Nov. 21st, physical signs the same;
temperature 103.5°; respiration 80. Nov. 22d, urgent dyspnoea; dulness
on percussion over top of right lung and over lower part of left lung;
is delirious; no perspiration; urine scanty; bowels freely open. From
this date the dyspnoea became more urgent, and death occurred at 4
P.M. on the 23d.
Autopsy by Dr. W. P. Northrup, curator: Body well nourished; slight
oedema of both legs; swelling at angles of jaws, most marked on left
side. Vessels of brain moderately injected; otherwise appearance
normal. Cicatrizing ulcers on both sides of fauces; a diphtheritic
pseudo-membrane on septum of nose, larynx normal. Trachea, upper half
apparently normal; a thin film of pseudo-membrane extends from just
above the bifurcation upward to nearly the middle of trachea. About an
ounce of fluid in each pleural cavity; on the right side a few loose
flakes of fibrin floating in the serum, and consolidation of lung at
apex; collapse in one or two places. Left side, recent adhesions over
whole of posterior surface and base; surface of lower lobe dark, and
when it is detached strings of fibrin adhere to it, and it is
consolidated. The cut surface shows marked oedema, injection, increase
of mucus in bronchi, and disseminated miliary tubercles in every part;
no tubercles in the pleura, and none elsewhere in the body except in
the left lung; tubercles in the lower lobe larger and more thickly
grouped than in the upper lobe. Decolorized clots in heart, extending
from ventricles into auricles of both sides. The capacity of the
ventricles seems normal. Liver and spleen, normal. Kidneys rather
large; capsules not adherent; superficial veins injected. The cut
surface shows congested pyramids and pale cortex; markings indistinct
and irregular; about four ounces of clear straw-colored fluid in
abdominal cavity, and the solitary follicles of {520} large intestines
show pigmentation; two simple intussusceptions, each three-fourths
inch in length, in small intestines.
Coryza frequently commences at or about the time of the pharyngitis.
The inflammation of the Schneiderian membrane is continuous
posteriorly with that of the fauces, and is announced by redness and
swelling, inability to breathe freely through the nostrils, and an
irritating ichorous discharge. Simple coryza in itself involves little
danger, though it is an unpleasant complication, and in the nursing
infant it may interfere with sucking. Diphtheritic coryza, on the
other hand, which is frequently present when diphtheria complicates
scarlet fever, involves danger, since it is apt to cause ulcerations,
hemorrhages, and septic poisoning. When the local symptoms are
unusually severe and the discharge abundant, it is probable that
inflammation has in some cases extended to the antrum of Highmore.
Inflammation of the middle ear is another unpleasant and not
infrequent complication. It is attributed to extension of the catarrh
from the pharynx along the Eustachian tube to the tympanum. In a
considerable proportion of cases of otitis media this tube is occluded
by the infiltration and swelling of its mucous membrane, so that the
muco-pus escapes with difficulty or is retained. Hence severe earache,
an increase of the febrile movement, and outward bulging of the
membrana tympani occur. Sometimes headache or other cerebral symptoms
arise, probably from the fact that the meningeal artery, which
supplies the meninges, is connected by anastomosing branches with the
tympanum. In one of the cases related above it will be recollected
that the ulceration and abscess extended from the fauces to the middle
ear, the entire Eustachian tube having disappeared in the ulcerative
process.
Frequently, the otitis escapes detection, its symptoms being masked or
obscured by the general disease, until the membrana tympani is
perforated and otorrhoea begins; but by careful examination the nature
of the complication can usually be ascertained before the ear is
injured to this extent, for a patient too young to speak will often
press with the fingers against the painful ear or lie with the ear
pressed upon the pillow, evidently having an increase of suffering if
placed in any other position. One old enough to speak and in proper
mental condition makes known the earache as soon as it occurs.
The mucous membrane of the tympanum, red and swollen from
inflammation, secretes muco-pus abundantly; and this, pent up in the
cavity, must obtain an exit before relief occurs. It is well if this
secretion escape, though with difficulty, down the Eustachian tube.
The destructive action of the pus upon the delicate structure of the
ear is often such that, within a few days, irreparable harm is done
and more or less deafness results. Relief can occur, if the Eustachian
tube remain closed, only by perforation of the membrane and the
discharge of the secretions into the external meatus. When this occurs
the inflammation in the most favorable cases gradually abates, the
aperture in the drum closes, and the integrity of the auditory
apparatus is preserved. In severe cases the mastoid cells
participating in the inflammation become filled with muco-pus and
tender to the touch, and often the collateral oedema causes
tumefaction and narrowing of the external ear, which subside with the
discharge of pus from the tympanum.
{521} Unfortunately, there is for many a more melancholy history--a
more destructive inflammation, involving permanent impairment or total
loss of hearing. This is especially apt to occur in strumous and
feeble children. All grades of inflammation and destructive action
occur in different cases. The perforation in the drum-membrane may be
large or the membrane may be completely destroyed, and the detached
ossicles escape one by one into the external meatus, and in a few
instances, fortunately rare, this occurs in both ears, producing
complete and permanent deafness. In my own practice this has never
occurred, but I have met one or two adults who were totally deaf from
this cause.
The mucous membrane which lines the bony wall of the middle ear has
the function of the periosteum, and therefore, when inflamed and
subjected to pressure, is liable to ulcerate. As in other parts of the
skeleton under similar conditions, superficial caries or necrosis of
the underlying bone is apt to occur. The carious or necrotic process
may extend to the mastoid cells. An offensive otorrhoea, continuing
for months or years, indicates the persistence of this pathological
state of the tympanum, which is rendered so obstinate by the presence
of dead bone. A moment's survey of the anatomical relations of the
middle ear shows the danger to which these patients are liable. A thin
bony septum, perforated with blood-vessels and sometimes containing
congenital apertures, separates the tympanum from the cranial cavity
above. Posteriorly lie the mastoid cells, connected with the tympanum
by one large and several small apertures. Anteriorly is the
commencement of the Eustachian tube and in close proximity to the
tympanum lies the carotid canal, and at one point also the superior
petrosal sinus. Virchow has shown how inflammation extending from the
ear in otitis media sometimes produces such compression of the veins
or sinuses by the swelling from the infiltration and exudation that
the circulation is arrested, and the fibrin contained in the blood of
these vessels is precipitated, forming thrombi, with the most
disastrous effect upon the individual. Pus may also burrow in the
interstices of the bone, causing great pain, or the pent-up
secretions, having no outlet for escape, may in time undergo caseous
degeneration, producing the conditions in which tuberculosis so often
originates.
Death not infrequently occurs in chronic otitis media in another way.
The otorrhoea, after months or years, suddenly ceases, the child
complains of constant severe headache and is feverish, and the case
ends in coma, preceded perhaps by convulsions. Meningitis has
occurred, produced by extension of the inflammation through the thin
bony septum which divides the tympanum from the cranial cavity, and at
the autopsy hyperæmia of the meninges, fibrin, pus, perhaps softening
of the brain and an abscess, are formed in the portion of the
encephalon adjacent to the tympanum. Therefore, otitis media, though
it often ends favorably, is in many patients an obstinate, dangerous,
and even fatal sequel of scarlet fever.
The complication known as scarlatinous rheumatism is regarded by some
as a synovitis, but its symptoms, especially its shifting from joint
to joint, seem to ally it to the rheumatic affections. In some
epidemics it is common. It usually begins toward the close of the
first week or in the second week, and its common seat is in the ankle,
phalangeal, and wrist joints. It is attended by very little swelling
in {522} most patients, though the joints are tender and painful on
pressure. It does not seem to retard convalescence materially, though
it produces suffering and involves danger as regards the heart. It
subsides in a few days with the ordinary treatment of acute
rheumatism, and even without special treatment, the chief danger being
that, as in idiopathic rheumatism, endocarditis may arise, with
permanent crippling of the valves. The following was a case of
valvular disease having this origin. It occurred in my practice.
_Case 5._--Freddy M., aged four years, sickened with scarlet fever
March 6, 1879. The usual vomiting occurred on the first day, and the
temperature was 104°. The case progressed favorably till March 14th,
when he complained of pain in both wrists, both ankles, and both
knees. On March 17th the general condition was good, the urine
contained no albumen, and apparently few urates, but he still had pain
in the joints of the upper and lower extremities and in the back;
pulse 140, temp. 103°; breathes with a slight moan; urates in the
urine, but no albumen. A distinct mitral regurgitant murmur is now
heard for the first time. Under the use of salicylate of sodium the
pain in the joints soon ceased, but the mitral murmur is permanent.
The following prescription is for a child of five years: