Alfred Martinet.

Clinical diagnosis, case examination and the analysis of symptoms online

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colic vein. 12. Ileocecal angle. 13. Appendicular veins. 14. Appendix.
75. Spleen. 16. Stomach (opened). 77. Intrahepatic tributaries of portal
vein. j8. Celiac axis. 19. Tail of the pancreas. 20. Pancreatic veins.
^i. Inferior mesenteric vein. 22. Mesocolon. 23. Descending colon. 24.
Colosigmoid vein. 2). Sigmoid flexure.



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750 SYMPTOMS,

4. The Ascites of Pylephlebitis. — An altogether exceptional
form characterized by its sudden onset, its exceedingly prompt
recurrence after puncture, the attendant pain, diarrhea, vomit-
ing, and hemorrhage in the digestive tract, the splenic enlarge-
ment, and the pronounced development of collateral circulation
in the abdominal wall.



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ASTHENIA AND [from a, privative; aOevogj strength^
FATIGUE. L Deprived of strength. J



The term fatigue relates to a sensation too commonly experi-
enced and well characterized to require definition. At most
need it be said that all grades of fatigue may be encountered,
from the mild, temporary, almost pleasant sensation of fatigue,
manifested in a desire to rest, to- deep, persistent, and lasting
exhaustion, almost completely depriving the individual of will
power and of the ability to act. Lastly, it is necessary to make
a distinction between "paralysis," or abolition of voluntary
movements of some portion of the body, and "fatigue," which
merely renders motion distressing or actually painful ; as a mat-
ter of fact, however, "paresis" is in some respects closely allied
to "fatigue."

Fatigue as a symptom is too common and ordinary a mani-
festation of most infectious, toxic, or depressive states to lend
interest even to an attempt at a complete semeiologic descrip-
tion in this connection. The scope of this chapter will there-
fore be restricted:

1. To recalling the commoner clinical states in which fatigue
occurs as a symptom.

2. To recalling under what circumstances fatigue, by virtue
of its unusual persistency, intensity, or variety, assumes definite
clinical significance and is sometimes practically pathognomonic.

The feeling of fatigue may be physiological, i,e,, normal, after
prolonged physical or mental exertion, after some form of shock
to the system, violent emotion, or prolonged test. In this in-
stance it is merely accidental and temporary. It yields readily
to rest, sleep, and removal of the cause.

Fatigue may assume an abnormal, pathologic type by virtue
of:

Its intensity (exhaustion, profound asthenia).

(751)



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752 SYMPTOMS,

Its duration (yielding neither to rest nor to removal of the
cause).

Its special modalities, being frequently periodic in type.

Its location, often in the lumbar regions.

It may be succinctly recalled that the more usual causes of
pathologic fatigue may be:

I. Nervous. — Nervous fatigue results naturally from over-
work, repeated emotion, and in particular from insomnia of what-
ever cause.

It is met with almost constantly, either as a subsidiary or
principal manifestation, in the majority of organic diseases of the
nervous system, and in particular in all paralytic states, to which
no further reference will be made.

Its diagnostic significance may be very great in all forms
of depressive psychoneuroses, zH:!,, neurasthenic and neurastheni-
form states, anxiety neurosis, cerebrocardiac neuropathy, psy-
chasthenia, general asthenia with gastrointestinal atony, ptosis,
and impaired nutrition, sympatheticotonia, etc. It is constant in
all these conditions and sometimes predominant and overmastering;
it is nearly always associated with insomnia. The cause will
always be found to be overstrain, physical or mental; sexual
excesses, or some emotional shock, the patient himself not gen-
erally connecting, however, the two groups of phenomena. Once
this cycle has been established, vis., excessive excitability ("emo-
tionalism,** suggestibility) and asthenia (insomnia), it tends, as
an actual vicious circle, to persist, the "emotionalism" and sug-
gestibility engendering or accentuating the asthenia and insom-
nia, and the asthenia and insomnia, in turn, engendering or ac-
centuating the "emotionalism" and suggestibility.

The diagnosis is generally easy, an inquiry into the patient's
mental state yielding conclusive results. It is to be borne in
mind, however, that a diagnosis of primary psychoneurosis
should never be made except after a process of exclusion, and
that the practitioner should always make certain that it is not
symptomatic of some somatic disorder such as tuberculosis,
arteriosclerosis, syphilis, azotemia, etc.



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ASTHENIA AND FATIGUE.



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754 SYMPTOMS.

n. The humoral caases of fatigue are legion. Any form
of intoxication, whether endogenous or exogenous and toxic or
toxinic, may cause asthenia. However defective the following
classification may be — and it must be confessed that many of
the groups overlap— it may be adopted, even if merely for mnemo-
technic purposes.

(a) Anemias. — In this group fatigue is continuous and is
associated with the customary indications of anemia, viz., pallor
of the mucous membranes, reduction of red cells, reduction of
hemoglobin, etc., together with anorexia, indigestion, etc. The
main object, however, should be, trace the cause of the anemia
(see Anemias).

(b) Hyposph3rxic States. — ^These involve a special circulatory
syndrome characterized essentially by low blood-pressure and
relatively high blood viscosity, these causing all the usual mani-
festations of impaired circulation, vis,, cyanosis, lowered super-
ficial temperature, dyspnea, and undue fatigability (see Low blood-
pressure).

(c) Conditions of Glandular Insufficiency. — Particular atten-
tion will here be paid to Addison's disease and myxedema.

1. Addison's disease (adrenal insufficiency). — Addison's disease
constitutes simply a very serious, but exceptional, form of adrenal
insufficiency, which recent observations, particularly those of Ser-
gent, have shown to be so common in, all infectious and post-infec-
tious states (typhoid fever, scarlet fever, dysentery, malaria, chol-
era, tuberculosis, etc.). During the course of these disorders the
3 cardinal signs should be systematically looked for: Asthenia,
low blood-pressure, and Sergenfs white line.

2. Myxedema. — ^The characteristic doughy infiltration of the
tissues (myxedema), the repeated intermissions in the progress
of the disease, and the permanent asthenia lead to the diagnosis.

(rf) Diathetic States (Metabolic Disorders).

1. Obesity. — This in itself is often dependent upon insufficiency
of several of the ductless glands, and particularly of the thyroid,
which allies it in some respects to myxedema. Asthenia should
lead to a suspicion of the latter condition (see Obesity).

2. Diabetes. — Ordinarily the diabetic is a supernormal, over-
active, indefatigable individual. Asthenia of unknown origin may.



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ASTHENIA AND FATIGUE, 755

however, at times lead to the detection of an incipient diabetes in
a previously healthy subject; acetonemia or azotemia will do the
same in a subject with glycosuria of long standing (see Glycosuria),
(e) Autotoxic States.

1. Uremia (and especially azotemia). — ^A persistent, overpow-
ering asthenia in conjunction with general torpor occurs almost
constantly in azotemia.

2. Arteriosclerosis (senile degeneration). — The same state-
ment 2q)plie& to arteriosclerosis.

III. The infectious causes of "fatigue" and asthenia mani-
festly induce them through poisoning of the nervous and mus-
cular tissues by toxins and through adrenal insufficiency.
Strictly speaking, they should therefore be included in the groups
already given. Let it be again repeated that in the classification
herein adopted *'dogmatic logic" is deliberately sacrificed in the
interests of "practical pragmatism."

The infectious forms of fatigue are often plainly evident ; this
applies to most of the asthenic conditions witnessed in conjunc-
tion with acute infections, e.g., typhoid and post-typhoid asthenia,
influenzal and post-influenzal asthenia, diphtheritic and post-
diphtheritic asthenia, etc. In any case careful inquiry should
be made to determine (1) whether this post-infectious asthenia
is not concealing incipient tuberculous disease, and (2) whether
It is accompanied by pronounced signs of adrenal insufficiency
(low blood-pressure, asthenia, Sergent's white line).

Particular attention should be paid to the chronic, sluggish,
cryptogenic forms of asthenia. In this connection especially
should the physician refuse to be satisfied with such "easy"
diagnoses as "anemia" or "neurasthenia," but should, on the
contrary, make a deliberate search for the three great chronic
infections (tuberculosis, syphilis, and malaria) and the three
main varieties of intoxication already referred to (uremia, gly-
cosuria, and hyposphyxia).

No detailed reference need be made to the well-known signs
of these disorders. Yet it may be recalled in conclusion that
any case of persistent, unaccountable asthenia should lead one
to the particular thought of the possibility of incipient tubercu-



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756



SYMPTOMS.



losis, evidences of which should be sought with great care,
vis., (1) Functional: weakness, lassitude, dyspnea on exertion,
anorexia, loss of weight, slight vesperal fever, night sweats, cough,
frequent heart rate, and hemoptysis. (2) Physical: reduced breath-
ing capacity, slight impairment of resonance at one apex, in-
creased vocal resonance, and persistent abnormalities of respira-
tion at one apex (rough, jerky breathing; rough, prolonged, and
blowing expiration; friction rubs, etc.).

Fluoroscopy, while of very great value, has in no wise de-
tracted from the significance of the above time-honored physical
signs.

Systematic clinical examination will automatically yield a
solution to these problems, provided it is, or attempts to be,
thorough and comprehensive.



Systematic Clinical Examination of Asthenic Subjects.



I. Determination of blood-
pressure, systolic and
diastolic

High blood-pressure.

Low blood-pressure.


Arteriosclerosis, nephritis, azotemia.
Hyposphyxia, tuberculosis, adrenal in-
sufficiency.


2. Blood examination.
Low red cell count.
Hyperviscosity.

Hyperazotemia.
Wassermann reaction.


Anemia.

Hyposphyxia, azotemia, tuberculosis,

adrenal insufficiency, acetonemia.
Azotemia.
Positive: Syphilis.


3. Temperature.
Hyperthermia.


Infectious states (tuberculosis, malaria,
etc.).


4. Auscultation.

Lungs.

Heart


Tuberculosis.

(Accentuation of second sound, gallop
rhythm: Nephritis, arteriosclerosis).


5. Urine examination.
Sugar, acetone.
Albumin.


Diabetes, acetonemia.
Albuminuria (azotemia).


6. Examination of reflexes
and nervous reactions.


1. Psychoneuroses.

2. Sergent's white line: Adrenal insuffi-
ciency.



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r%xjjT T c {French: Frissons, from frigere,]



A chill consists essentially of a sudden tremor of varying ex-
tent and varying duration, usually accompanied by a sensation
of cold and followed by a sensation of warmth.
At least three grades of chills may be recognized :
Cryesthesia or chilliness^: An unpleasant sensation of cold, with
very slight tremor.
Shivering,

An actual major chill, involving the entire body and attended
with chattering of the teeth, diffuse and violent trembling, and an
intense feeling of cold.

All true chills, except the nervous or emotional chills, are
followed by fever. As a general rule, a definite chill accom-
panied by an abrupt rise of temperature is symptomatic of the
onset of an infectious disease, by far the most frequent of such
disorders being pneumonia, grippe, malaria, tonsillitis, and sep-
ticemia.

The commonest causes of chills may be enumerated as fol-
lows :

Pyogenic and septicemic infections :
Pneumonia, tuberculosis, appendicitis.
Septic wounds.
Suppurative disorders of the liver and kidneys; biliary and

urinary infections.
Tonsillitis.

Vegetative endocarditis.
Phlebitis,
Empyema.
Erysipelas,
Malaria.

Renal and hepatic colic.
Nothing special need be said concerning:

(757)



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758



SYMPTOMS,



The chill from exposure or "a frigore,"

The emotional chill, or shivering "with fright" or "with horror/'
or simply the psychoneuropathic chill. Some nervous degen-
erates, apparently "constitutional shiverers," are always ready
to shiver on the slightest provocation.



Causes.


Fbykb.


BLOOD Ex-


Clinical


MEANS or






amination.


SIGNS.


lUCOYKBT.


Nervousness.


None.


Negative.


Neuropathic
stigmata.


Suggestion.
Discipline.


Septic states.


Remittent


Polymor-


Local or deep-


Dressings,






phonuclear


seated vis-


operation, and






leucocy-


ceral infec-


drainage.






tosis.


tion.

Infectious en-
docarditis.


Collargol in-
jections.


Phthisis.


Remittent.


Frequently


Stethoscopic


General and






leucocy-


and fluoro-


local treat-






tosis.


scopic pulmon-
ary evidences.

Tubercle bac-
illi in sputum.


ment. Hy-
gienic meas-
ures.

Spontaneous
recovery.


Pneumonia.


Continued.


Frequently


Stethoscopic


Hygienic treat-







leucocy-


evidences.


ment. Gen-






tosis.


Characteristic
sputum.


eral measures.
Spontaneous
recovery.


Hepatic colic.


Remittent


Not char-


Hepatic colie


Morphine.




or inter-


acteristic.


or gastralgia.


Operation.
Diet




mittent




Frequently








jaundice.










Pain in right










hypochon-










drium.




Malaria.


Intermit-


Leucopenia.


Splenic enlarge-


Quinine.




tent (at-


Malarial


ment


Arsenic.




tacks at


parasites.








definite in-










tervals).








Tsrphoid fever.


Continued.


Leucopenia.


Typhoid state.


General treat-






Agglutina-


Rose spots.


ment






tion test


Splenic enlarge-


Diet.






Blood cul-


ment, etc.


Cold baths.






ture.







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nnuiA \X(i(ia. Drowsiness J suspension]

i^UMA. 1^ ^y ^^^ mental fv/nctions. J



Coma consists of a state of profound somnolence with more
or less complete loss of consciousness, sensibility, and motility.
While it is the most striking feature of the syndrome resulting
from apoplexy, it may be and frequently is met with under other
circumstances.

It could hardly be confused with the deep sleep of convales-
cents or hysterical cases, or with syncope or asphyxia.

The deep sleep of convalescents is a quiet sleep, with the
pulse regular and respiration normal. It is seldom so profound
that the patient cannot be awakened by some sharp stimulus,
and the history of the case will generally exclude the idea of
coma.

The sleep of hysterical patients might more readily lead to
confusion. Only rarely, however, will the previous history and
the features of the onset of the attack fail to point the way to
a proper diagnosis, which will be thoroughly illuminated, fur-
thermore, by systematic investigation of the hysterogenous
zones.

Systematic diagnosis of hysterical pseudo-coma may be said
to be based on the following clinical findings:

1. If the onset was sudden, the patient falling, this fall oc-
curred without the patient receiving any severe blow or any
wound or traumatism; no biting of the tongue, and no relaxa-
tion of the sphincters. •

2. Frequently there are noted contracture, winking of the
lids, and various movements of the eyeballs, which are absent
in true coma.

3. The patient, while apparently insensitive to pain, noise,
and light, reacts to an exaggerated degree, on the other hand,
to pressure upon a hysterogenous zone, to a cold affusion, or
to appropriate suggestion in a loud voice. The author has wit-

(759)



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760 SYMPTOMS.

nessed many seizures of this type, sufficiently striking to alarm
an experienced hospital staff, suddenly cease upon suggestion
that the patient was to be "immediately placed in isolation in
the special quarters" or to be "subjected to cauterization with
the hot iron." Much oftener, indeed, it yielded to brief occlusion
of the nose and mouth.

4. Lastly, these hysterical pseudo-comatose states are fre-
quently associated with postures apparently unconsciously as-
sumed, but plainly semi-voluntary to the close observer; the
same applies to the pseudo-delirium encountered in these sub-
jects.

S3mcope is ordinarily of short duration. The sudden loss
of consciousness, pallor, weakness, and even almost complete
arrest of the heart-beats, the rapidly beneficial effect of the hori-
zontal posture, elevation of the legs, and stimulating injections,
will preclude any prolonged hesitation.

In asphyxia, the history of the case, the cyanosis, the livid ap-
pearance, and the reduced temperature of the lower extremities
will obviate any mistake.

The ordinary causes of coma may, for practical purposes,
be enumerated as follows:

Toxic causes: Exogenous: Alcohol, opium.

Endogenous: Uremia, acetonemia, acidosis
(diabetes).

Cerebral causes: Vascular: Apoplexy, hemorrhage, throm-
bosis, or epilepsy.

Inflammatory : Meningoencephalitis.
Neoplastic : Brain tumors.
Traumatic: Skull fractures.

Infectious causes: Malaria, rheumatism, typhoid fever, or in-
fectious jaunSice.

Circulatory causes: Stokes- Adams' disease.

Coma having been clinically encountered, the causal diag-
nosis, which is of prime importance both because of the prog-
nosis it affords and the indications it gives for treatment, is
based chiefly upon the history of the illness and, in particular, on
the results of clinical examination. The history and clinical findings
must be systematically collated.



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COMA. 761

The history is of prime imfrortance,

1. Has there been some traumatic injury, fall, or contusion
preceding the coma? If so, fracture of the skull.

2. Does the patient give a history of similar seizures before,
and is he subject to convulsive attacks? Epilepsy, eclampsia,
uremia.

3. Has the patient been intemperate? Had he been on an
alcoholic spree before the coma came on? Alcoholism.

4. Has the patient had syphilis? Has he previously had treat-
ment for this disease? Was he under treatment at the time?
Brain syphilis.

5. Did the patient have nycturia, vertigo, albuminuria, etc.?
Interstitial nephritis, arteriosclerosis, uremia, etc.

6. Was the patient in a rundown state; did he pass very
much water; had he had itching and digestive disturbances for
a few days, etc? Diabetes.

And so on . . .

In short, the practitioner should <:arefully take note of all
information supplied by the relatives as to the patient's previous
medical history ; such information will often yield highly service-
able clinical indications.

The direct clinical examination is of much greater importance
stUL

As in other conditions, it should be conducted systematically
and comprehensively. The following lines of inquiry are, how-
ever, particularly essential:

1. Is hemiplegia present? (See Hemiplegia), With decrease of
muscle tone on one side of the body ; sometimes conjugate devi-
ation of the head and eyes, an exaggerated patellar reflex on one
side, and the Babinski ^ sign or plantar reflex. Hemiplegia, if
present, will usually constitute a clinical expression of brain
hemorrhage or softening; it may be met with in uremia, and
in some forms of meningitis in childhood.

2. Is fever present? And if so, was it present before the
coma (typhoid fever, cerebral rheumatism, tuberculous menin-
gitis, cerebrospinal meningitis) ? Or was it present along with
the coma (pernicious malarial fever) ? Or did it come on after
the coma (certain forms of cerebral hemorrhage) ?



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762



SYMPTOMS.





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764 SYMPTOMS.

3. Is sugar or albumin present in the urine? The presence
of sug^r would suggest diabetic coma; in' this case the exami-
nation should be supplemented by tests for acetone and diacetic
acid and by a determination of urinary acidity (see Technical



Online LibraryAlfred MartinetClinical diagnosis, case examination and the analysis of symptoms → online text (page 8 of 50)