[Guides to Therapy for Medical Officers]
[From the U.S. Government Publishing Office, www.gpo.gov]

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Document TM 8-210
Reserve
WAR DEPARTMENT
TECHNICAL MANUAL
GUIDES TO THERAPY FOR
MEDICAL OFFICERS
March 20, 1942
non -circula ting

ell
TM 8-210
C 1
TECHNICAL MANUAL
GUIDES TO THERAPY FOR MEDICAL OFFICERS
Chang es ] WAR DEPARTMENT,
No. 1 J Washi ng to n , May 6, 1943.
TAI 8-210, March 20, 1942, is changed as follows:
17. Burns.
*******
1). Fundamentals of treatment.
(2) Proper prophylactic measures * * * should be taken. Satisfactory
end results, that is, minimal scar formation, largely depend on the avoidance
of pyogenic infection; the moist surfaces of burns provide ideal conditions for
bacterial growth, and it is therefore of paramount importance to employ, if
possible, strict aseptic technic in operating on and dressing burns.
(3) To relieve pain.
c. Treatment.— (1) General—(a) Proper steps for the prevention or treatment
of shock (par. 15) should be instituted. In the presence of extensive burns,
quantities of plasma up to 12 units may be required in the first 24 hours. If
available, concentrated normal human serum albumin in appropriate amounts
may be used likewise. Transfusion of fresh whole blood is often needed to
combat the rapidly developing severe anemia which follows extensive burns;
when anemia exists, whole blood transfusion is particularly indicated as a
preliminary to skin grafting. Parenteral fluid replacement other than that
attained by means of plasma or whole blood transfusion should be accomplished
by means of 5 percent glucose in sterile distilled water. The intravenous
administration of sodium chloride solution should be reserved for
those burn cases in which mineral depletion is pronounced, as when great
loss of electrolytes occurs as a result of persistent vomiting.
(b) In all cases with moderate to severe burns, prophylactic chemotherapy
should be administered. Sulfadiazine is the drug of choice (sulfanilamide may
be substituted) with an initial dose of 4.0 grams (60 grains). Subsequent
doses of sulfadiazine should be given only under the direction of a medical
officer. It should be kept in mind that although sulfonamide therapy may
serve to prevent infection, great care must be exercised in employing such
therapy in burn cases. The extensive fluid loss and possible kidney damage
so common in burn cases increases the danger of renal complications from
sulfonamide therapy. Maintenance doses of sulfadiazine should be given
in 0.5 gram (7}£ grains) doses every 4 hours until such time as adequate
kidney function can be demonstrated, under which circumstance the dosage
may be increased to 1 gram (15 grains) every 4 hours.
(c) Prophylaxis against tetanus (par. 49) is indicated in all patients with
second or third degree burns.
(d) A prophylactic dose of gas-bacillus antitoxin (par. 48) may be given
at the discretion of the medical officer.
523003°—43------ 1 UTSU LIBIMY
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(e) Pain should be relieved by adequate doses of morphine. Pain resulting
from an extensive burn can ordinarily be relieved by a dose of grain
of morphine. In the presence of pronounced anoxia large doses of morphine
are dangerous, and under such circumstances the dose should not exceed 14
grain.
(2) Emergency treatment of the burned area.—(a) The burned surface
should be covered with a liberal amount of boric acid ointment, or if this is
not available, with vaseline. The burn should then be covered with strips
of a sterile fine mesh gauze (44 mesh gauze bandage is satisfactory). Over
this should be added a smooth thick layer of sterile gauze dressing (large or
small first aid dressings are especially suitable for this purpose). Finally,
a gauze or muslin bandage should be firmly applied over the dressings.
(b) Contamination of burned surfaces by organisms from the nose and
throat is responsible for most of the more serious infections which subsequently
develop. Therefore, to minimize contamination from this source,
masking should be practiced by the surgeon and assistants. If masks are
not available, mouths should be kept closed.
(c) The prompt administration of plasma, when feasible, constitutes an
important element in the emergency treatment of burns.
(3) Definitive treatment of the burned area.—The burned area should be
treated as follows, standard operating room technic, if possible, being employed,
with the patient, as well as all attendants, fully masked:
(a) Ether, benzene, lard, or other detergents should be used to remove
grease, if present. The burned area and then, separately, the surrounding skin
are to be carefully cleansed, using neutral soap and water; green soap should
not be used. Avoid the use of brushes in the cleansing of the burn.
(b) All blisters and loose shreds of epidermis are carefully removed, and this
material is saved for bacteriologic study, if feasible. Skin that gives evidence
of irreparable damage through its full thickness should be excised (evidence of
irreparable damage to deeper layers of skin may .not be apparent for several
days, and excision in such cases should be done as a secondary procedure).
The resulting wound should be handled like any other open surgical wound, primary
grafting of skin being carried out, if conditions permit. For painful
surgical procedures or dressings, general anesthesia, preferably obtained by intravenous
injection, should be employed.
(c) Burns of surfaces of any portion of the body may be treated with boric
acid ointment. After thorough surgical cleansing, the burned area should
be covered with a generous application of boric acid ointment. Strips of
a fine mesh sterile gauze (44-mesh gauze bandage is satisfactory) should be
applied. Over this should be added a smooth, thick layer of sterile dressing;
this may consist of gauze, absorbent cotton, cotton waste, or cellulose. The
dressings should be held in place by an evenly and firmly applied bandage;
stockinette or some form of elastic bandage is more effective than the ordinary
roller bandage. The dressing should not be disturbed for 10 days unless
complications develop. Firm pressure is especially important in the case of
burns of the hands and face. Immobilization of the part by splinting should
be effected when feasible.
(d) As an alternate method of definitive treatment, burns of all surfaces
except those of the hands, face, genitalia, and those involving the circum-
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GUIDES TO THERAPY FOR MEDICAL OFFICERS C 1
ference of an extremity may be treated with, tannic acid and silver nitrate.
This method, however, should not be employed in the instance of burns which
are grossly contaminated or in which 12 or more hours have elapsed since
the receipt of the burn. A freshly prepared 10 percent aqueous solution of
tannic acid is sprayed over the burned area. This is followed immediately by
spraying the area with a mixture of equal parts of 10 percent tannic acid and
10 percent silver nitrate solutions. This mixture should then be sprayed on the
burn every half hour until a satisfactory eschar has been formed. Care should
be taken to avoid spraying normal skin about the wound. While drying, the
burned area may be kept exposed to the air in a heated cradle. After the eschar
is dry, it may be covered by a dry sterile dressing. In the absence of infection,
the eschar should be allowed to separate spontaneously. If infection develops,
the eschar must be removed from the entire infected area, and the latter should
then be treated like any other infected wound, with the employment of appropriate
systemic and local therapy (par. 51).
(e) Physiological saline solution has been found useful in the treatment of
burns involving the face, hands, and especially fingers, the flexures, and the
perineum. It may also be used for the treatment of surface infections following
the removal of eschars produced by tannic acid or other agents. Saline may
be employed in the form of packs or baths.
[A. G. 062.11 (3-23-43).] (C 1. May 6, 1943.)
24. Care of feet.—a. Foot hygiene.
* * * * * * * *
(4) Excessive moisture plays * * * wear oiled shoes. The Army foot
powder is of value. It is composed of salicylic acid 2 percent, desiccated alum
1 percent, starch 10 percent, talcum powder 78 percent, boric acid 6 percent,
and zinc stearate 3 percent. The powder is rubbed on the feet and used as
a dusting powder for the feet and socks.
* * * * * * *
b. Trichophytosis.— (1) Proper cleansing and the control of moisture greatly
reduce the incidence of so-called “athlete’s foot.” Prevention of infection in
company bathhouses may be attempted by requiring a foot bath of a few minutes
in a solution of calcium hypochloride or sodium hypochloride giving 50 to 100
parts per millim of available chlorine. The Army foot powder is an efficient
preventive agent if rubbed on the feet and used as a dusting powder for the
feet and socks once or twice daily.
*******
[A. G. 062.11 (3-23-43).] (C 1, May 6, 1943.)
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GUIDES TO THERAPY FOR MEDICAL OFFICERS C 1
Section IV is rescinded and the following substituted therefor:
Sect ion IV
DIAGNOSIS AND TREATMENT OF VENEREAL DISEASES
Paragraph
General______________________________________________________________________ , 36
Gonorrhea--------------------------------------------------------------------------------------------------------- 37
Syphilis_______________________________________________________________________ 38
Chancroidal infection---------------------------------------------------------------------------------------- 39
Lymphogranuloma venereum------------------------------------------------------------------------------ 40
Granuloma inguinale------------------------------------------------------------------------------------------ 41
36. General.—a. This section on the diagnosis and treatment of venereal
diseases is based on the opinions and recommendations of the Subcommittee on
Venereal Diseases of the Committee on Medicine, Division of Medical Sciences,
National Research Council. Since substantial changes from previous treatment
■methods are here recommended, this section should be read carefully by all
medical officers who are called upon to treat venereal diseases. It is published
as a general guide for medical officers and is to be used with due consideration
of factors which may be presented by each individual case. It is not intended
that the recommendations contained herein will be used to the exclusion or
neglect of other indicated therapeutic or nursing procedures.
b. In the zone of the interior and in the communications zone venereal disease
cases will ordinarily be hospitalized for treatment during the infectious stages.
In order to maintain effective strength of organization during combat, consideration
may be given to the treatment of venereal disease cases on a duty status
with their organization in the combat zone.
37. Gonorrhea.—a. Diagnosis in male.— (1) A diagnosis of gonorrhea must
not be made in the absence of laboratory confirmation. Treatment for gonorrhea
should be started at once if the patient has an acute purulent urethral discharge,
but material should be obtained before treatment is begun for subsequent
laboratory study (smear and/or culture).
(2) Acute gonorrhea.—The detection of gram-negative intracellular diplococci
in smears of the urethral exudate, or smears of the centrifuged sediment
of the first glass of urine, or fluid from conjunctival sac or joints, establishes
the diagnosis of gonococcal infection. In competent hands cultures yield a higher
percentage of positive results and are of particular value in cases in which no
gonococci are found in the smear.
(3) Chronic gonorrhea (posterior urethritis, prostatitis, seminal vesiculitis,
epididymitis, and arthritis.)—The detection of gram-negative intracellular diplococci
in smears of the exudate obtained by digital stripping of the prostate,
Cowper’s glands, and the urethra, or in smears of the centrifuged sediment’ of
urine passed after stripping the prostate, Cowper’s glands, and the urethra, or
the demonstration of gonococci in cultures of material so obtained, establishes
the diagnosis of gonococcal infection.
b. Diagnosis in female.— (1) A diagnosis of gonorrhea must not be made in
the absence of laboratory confirmation. (Treatment for gonorrhea should be
started at once in women who have evidence of this disease, even though laboratory
studies are negative or not available. If laboratory facilities are not
available, material for subsequent laboratory studies should be obtained before
treatment is begun.)
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(2) The detection of gram-negative intracellular diplococci in smears of material
obtained from any of the following: the urethra, Skene’s glands, or the
cervix (or from Bartholin’s glands or the rectum, when clinical symptoms exist) ;
or positive cultures of such material establishes the diagnosis of gonococcal
infection. (Caution: The normal genital bacterial flora and the flora of nonspecific
infections may contain organisms that in smear closely resemble gonococci.
Therefore, cultural methods should be utilized when possible.)
o. Gonorrheal ophthalmia.—The diagnosis is made on the basis of an acute
purulent conjunctivitis, pus containing gonococci, and rapid involvement of the
external coats of the eye. (Sulfonamide therapy should be instituted immediately.
Prompt ophthalmological consultation is imperative.)
d. Serologic tests for syphilis.—All patients with gonorrhea should be given a
serologic test for syphilis on admission, a test before being discharged to duty,
and if possible, a final test 2 months after discharge.
e. Treatment of gonorrhea in males and females.—(1) Local treatment of any
kind (injections, irrigations, massages, instrumentations) is contra-indicated in
uncomplicated acute gonorrhea.
(2) Treatment should consist of not more than two courses of chemotherapy.
A careful inquiry should be made as to previous sulfonamide therapy, recent
self-administered chemotherapy for gonorrhea, and for previous drug reactions.
(See par. 42.)
(a) Sulfa thiazole and sulfadiazine are each highly efficient, and in the doses
recommended cause toxic manifestations very infrequently. Either of these compounds
is recommended. Sulfapyridine, although nearly as efficient as sulfathiazole
or sulfadiazine, is more toxic and should be used only if the other compounds
are not available. Sulfanilamide is far less effective than the other sulfa compounds
in gonorrhea and is not recommended.
(&) The recommended dosage for sulfathiazole and sulfadiazine is 1 gram (15
grains) four times a day for 5 days. The recommended dosage for sulf a pyridine
is 1 gram (15 grains) three times a day for 5 days.
(c) A second course of the drug, in the same dosage, should be given if there
is evidence of persistence or recurrence of the disease. There should, however,
be a lapse of 5 days between the two courses of medication.
(d) Patients in whom the gonococcus is present after the second course, or who
have not made a satisfactory clinical response, generally should be transferred to
a general hospital.
(e) In males, local treatment to the urethra generally should be administered
only in a general hospital.
(f) In the female, hot vaginal douches (under no more than 2 feet of water
pressure) afford comfort and promote cleanliness. Acute pelvic inflammatory
disease is an indication for bed rest, ice bags to the abdomen, and analgesics. If
enemas are necessary, preliminary bathing of the perineum is indicated before
inserting the rectal tube in order to avoid inducing gonococcal proctitis.
f. Treatment of sulfonamide-resistant gonorrhea in males and females (general
hospitals).— (1) It is recommended that carefully selected patients with sulfonamide-
resistant infections be given 10 hours of sustained fever therapy, where such
therapy is available, preceded by chemotherapy consisting of sulfathiazole, 1 gram
every 6 hours for eight doses. This program should be preceded by 1 week of freedom
from sulfonamide therapy. Patients who are not subjected to this form of
treatment, and those who are not cured by this means, should be placed upon local
treatment.
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(2) Local treatment in male (sulfonamide-resistant cases only).— (a) When
the infection is confined to the anterior urethra, an anterior urethral injection,
once daily, of not more than 6 cc of a 5 percent solution of mild protein silver
or 0.5 percent of strong protein silver is advised. (Retain for 5 minutes.) It
should be kept in mind that prolonged use of chemicals tends to perpetuate urethral
discharge. Discharge caused by overtreatment of this type may be recognized by
the presence of many epithelial cells.
(&) All urethral injections are to be administered by a medical officer or a
trained attendant; not by the patient.
(c) Stop all local treatment if the patient develops acute symptoms of posterior
urethral infection, such as urgency, painful or marked frequency of urination, or
perineal or rectal pain; and confine treatment to hot Sitz baths. When acute
symptoms have subsided, resume anterior urethral injections and continue them
until prostatic stroking is begun.
(d) Extremely gentle prostatic stroking should be tried when the second glass
of urine has been clear, and the first glass nearly so, for 2 weeks. If gentle
massage is painful or causes a recrudescence of other symptoms, it should not
be repeated for 1 week, or until the symptoms have subsided. If it is not painful
and if no recrudescence of symptoms occurs, the gland should be gently stripped at
3- and 4-day intervals, and smears of the prostatic secretion examined every 2
weeks. (When prostatic massage is instituted too soon or applied too vigorously
it often induces complications and retards cure.)
(e) Infections of Cowper’s glands should be searched for in resistant cases.
If these glands are palpable, they should be gently kneaded. This can be accomplished
at the time prostatic massage is practiced, by placing the thumb
against the perineum and gently massaging first one and then the other gland
with the index finger.
(/) No instruments of any type should be passed into the urethra while
gonococci are present.
(3) Local treatment in female.— (a) See paragraph 37e (2) (f).
(b) The persistence of infection in Skene’s glands, Bartholin’s glands, or the
endocervical glands in spite of the use of measures recommended above constitutes
a special problem beyond the province of this directive. Such patients
require skilled gynecological treatment.
g. Determination of cure in male (iincomplicated cases).— (1) Cure is determined
by the inability to demonstrate gonococci in any of the urogenital fluids
including prostatic secretions, by smears or cultures.
(2) Patients whose symptoms have disappeared as the result of sulfonamide
medication may have the first test of cure on the third day after disappearance
of symptoms. Thus, for example, patients clinically well on the third day of
chemotherapy, whose urethral cultures or smears are negative for gonococci,
may have on the sixth day prostatic massage and may then be discharged to
duty if smears of the urogenital fluids are normal. When feasible, these
patients should return to the hospital for two subsequent examinations at
weekly intervals and should be discharged as cured after three negative
examinations.
h. Determination of cure in male (sulfonamide-resistant cases).—(1) Cure is
determined by the inability to demonstrate the gonococcus in any of the urogenital
fluids by repeated smears or cultures. Material for these studies should be
obtained in the manner described in paragraph 37a (3). The prostatic secretion
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should be included in the study of al! types of infection. Three successive
negative studies at weekly intervals constitute practical evidence of cure. Tests
for cure may be carried out after the patient has returned to duty.
(2) Patients whose symptoms disappear as the result of fever therapy may
have tests of cure stated on the second day following the treatment.
i. Determination of cure in the female (uncomplicated cases).—(1) Patients
whose symptoms have disappeared as the result of chemotherapy may have tests
of cure begun on the third day after disappearance of symptoms.
(2) Cure is determined by—
(a) Absence of tender masses or points of tenderness in the pelvis.
(b) Inability to demonstrate the gonococcus by smears or cultures in material
obtained from the urethra, Skene’s glands, Bartholin’s glands, or the cervix.
Such tests should be repeated every 2 weeks for 3 months, and, if all are found
to be negative, the patient should be discharged from observation. These
tests should be carried out on an ambulatory basis.
(c) To obtain material for smears and cultures, massage the urethra, Bartholin’s
glands, and Skene’s glands, obtaining secretion with small cotton-wrapped
applicator or a platinum loop. Pass bivalve vaginal speculum without lubricant,
expose cervix, clean vagina and cervical canal, squeeze cervix between ends of
speculum blades, and obtain expressed fluid on cotton applicators or platinum
loops for smear and culture.
j. Determination of cure in female (sulfonamide-resistant cases).— (1) Patients
whose symptoms have disappeared as the result of prolonged artificial fever
may have tests of cure begun on the second day after treatment. The tests of
cure are the same as those recommended for female patients in uncomplicated
gonorrhea.
(2) Patients under local treatment should have smears and culture done at
least every 2 weeks. If these tests remain consistently negative for 3 months,
and if there are no demonstrable complications, the patient should be discharged
from observation.
38. Syphilis.—a. Diagnosis of syphilis.— (1) It is of the utmost importance
that the diagnosis in early syphilis (primary and secondary stages) be established
at the earliest practicable moment and that treatment be instituted as soon as
the diagnosis is made.
(2) All ulcerative genital lesions, extragenital lesions characterized by indolence,
induration, and regional lymphadenopathy, and cases of urethritis
accompanied by indolent enlargement of related lymph glands are to be regarded
as probable cases of syphilitic infection until this possibility has been excluded
by repeated darkfield examinations and repeated serologic tests. In these cases
routine serologic tests will be done not less often than—
(a) On admission to sick report.
(&) Second week.
(c) About the end of the first month.
(d) About the end of the second month.
(3) Routine serologic tests will also be made in all cases of gonorrhea at
least as often as follows:
(a) On admission to sick report.
(&) Before return to a duty status.
(c) About the end of the second month.
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(4) Antisyphilitic treatment will not be started until the diagnosis of syphilis
is definitely established. The demonstration of the Treponema pallidum by darkfield
examination is conclusive as to the necessity for the immediate institution
of treatment. A persistent completely positive serology even in the absence of
confirmatory clinical signs or a history of infection is also diagnostic of syphilis,
and usually is an indication for treatment. Positive serologic tests on a single
specimen should never be made the basis of treatment in the absence of unmistakable
clinical evidence of syphilis. A completely positive precipitation or
complement fixation test (Kahn or Wassermann) confirmed by a positive complement
fixation test (Wassermann) on a second specimen indicates syphilis
provided no negative reactions have been obtained. Acute infection, particularly
malaria and possibly vaccination procedures, are believed to give rise at times
to transient false positive serologic tests. The presence of these complicating
factors should be excluded before making a definite diagnosis of latent syphilis.
In the event of incompletely positive or contradictory serologic reactions the
test should be repeated until the possibility of technical error is excluded.
b. Treatment of syphilis.— (1) General principles of treatment.— (a) No treatment
is to be given for suspected early syphilis until the diagnosis is made either
by darkfield examination or confirmed serologic tests. No therapeutic tests are
to be used.
(&) Arsenoxide (mapharsen) will be used as the standard arsenical. Neoarsphenamine
or other arsenicals cannot be substituted in the treatment schedule
outlined in table I.
(c) If it is necessary to use neoarsphenamine, because of the nonavailability
of arsenoxide, the former drug should be given only at weekly intervals in courses
of not more than 8 consecutive weekly doses.
(d) Tryparsamide and fever therapy are not to be used outside of a hospital.
(e) Each treatment is to be recorded on the Syphilis Register of the patient
or if for any reason a syphilis register is not available, a written record is to be
kept and transferred to the standard form as soon as possible. Each entry
will include date, drug, dose, and reaction.
(/) It cannot be too strongly emphasized that regularity of treatment schedule
without long or short time variations or lapses is critically important to both
infection, control, and cure. Every effort must be made to impress this fact
on enlisted men and officers as well as medical personnel.
(. Geographical distribution.—Occurs in most areas where malaria is hyperendemic.
c. Recognition.—Onset sudden, with persistent fever. The three cardinal
symptoms are hemoglobinuria, fever, and icterus. Temperature may reach 102° F.
to 103° F., usually accompanied by chill. Other symptoms are repeated vomiting
of bile-stained fluid, abdominal pain, jaundice or subicteric sclerae, enlarged
tender liver and spleen, severe prostration, progressive severe anemia, elevated
plasma bilirubin, with an increased indirect Van den Bergh reaction which may
later become direct. There is usually some degree of urinary suppression.
Color of urine may vary from light red to black (hemoglobinuria). Asexual
forms of P. falciparum usually absent from peripheral blood within 2 to 3 hours
of onset. Crescents and forms of tertian and quartan may be present. There
may be urinary suppression due to precipitation of acid hematin in renal tubules.
This may occur early and suddenly, and is the commonest cause of death, if
not corrected promptly. Cardiac failure is a common cause of death in posthemolytic
period. Other complications: grave anemia, hyperpyrexia, uncontrollable
vomiting, hiccough, sudden drop in temperature, prostration, and coma.
d. Specific diagnosis.—None. P. falciparum may be found in blood smears
taken either before or after, but rarely during an attack.
e. Treatment.— (1) Do not give quinine or atabrine until convalescence from
the attack of blackwater fever is established.
(2) Absolute rest. Keep patient warm. Whenever possible, treat the patient
at the place where he was taken ill until definite improvement occurs.
(3) Give a minimum of 2,060 cc of fluids per day and up to 6,000 cc if possible.
Volume of urine should be 1,200 to 1,500 cc per 24 hours. If unable to void,
catheterize every 4 hours in order to determine urine output and reaction to
litmus.
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(4) Immediate transfusion of whole blood if the patient is not anuric. This
may be repeated daily as indicated by persistence of severe hemoglobinuria or
severe anemia and asthenia.
(5) During period of vomiting, if urine is acid or if anuria exists, give
1,000 cc of sodium bicarbonate solution intravenously as described under cholera
treatment. Repeat after 12 hours if urine remains acid. When vomiting is
controlled, if urine is acid give sodium bicarbonate 0.6 gram (10 grains) by
mouth every 1 to 2 hours until urine is alkaline to litmus, and thereafter in
sufficient amounts to maintain slightly alkaline reaction.
(6) If plasmodia are found in blood smear after convalescence, give atabrine
0.1 gram the first day, two 0.1-gram doses the second day, and three 0.1-gram
doses the third day. Continue this dosage for 5 additional days. Watch for
recurrence of hemoglobinuria, as atabrine has occasionally precipitated an
attack.
f. Prevention.—(1) Adequate treatment of malaria cases, especially when due
to P. falciparum.
(2) Change of residence to temperature climate if feasible. Blackwater fever
often recurs if patient remains in a malarious region.
(3) Recognition of preblackwater state is important. Characteristics: toxic
appearance, slight jaundice, enlarged tender liver, dark-colored urine due to excessive
urobilin. Supplement antimalarial therapy with alkalis to maintain the urine
alkaline.
71. Oroya fever.—a. Etiologic agent.—Bartonella bacilliformis. The chronic
stage of oroya fever is verruga peruana. The acute stage as a rule and sometimes
both stages together are referred to as bartonellosis.
&. Geographic distribution.—Endemic areas are confined to hot, narrow valleys
of Peru, Ecuador, and Colombia, and possibly northern Chile and western Bolivia,
at altitudes from 1,500 to 9,000 feet.
c. Transmission.—The causative agent probably is transmitted by sandflies of the
genus Phlebotomus, biting principally at night from January to April. Native
dogs with bartonellosis may be an animal reservoir of infection.
d. Recognition.— (1) Early, acute stage (oroya fever).—Incubation period is
about 3 weeks. Insidious prodromal period is usually characterized by malaise
and low fever. Course of disease is then severe, with high, irregular, remittent
fever. Marked anemia develops rapidly, with intense pain over the long bones.
Death occurs in 10 to 40 percent of cases during the second or third week of the
disease.
(2) Late, chronic stage (verruga peruana).—Generally follows attack of oroya
fever by 30 to 60 days, or more, but may occur without an oroya fever stage. Initially
there is fever. Severe rheumatic pains frequently occur. Miliary (lenticulate
or nodular, often granulomatous) eruption develops on the face, trunk, and
extensor surface of extremities. Lesions may develop on all mucous surfaces
and the lesions may bleed freely or become gangrenous. Mortality is nil.
e. Specific diagnosis.— (1) Oroya fever.— (a) Identification of organism in
stained blood films.
(b) Blood culture.
(2) Verruga peruana.— (a) Usually history of preliminary attack of oroya
fever.
(&) Characteristic lesions.
f. Treatment.—There is no specific treatment. Multivitamin capsules and iron
should be administered during convalescence.
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g. Prevention.—In endemic areas avoid unnecessary exposure to bites of sandflies,
especially at dusk and dawn. Sleep under fine mesh bed net. Spray tents
and quarters, and especially the bed net, with pyrethrum insecticide at dusk.
Apply approved mosquito repellent skin lotions, as these are also effective against
sandflies. In some endemic areas it may be feasible to plan travel so as to camp
nt night at an altitude above 9,000 feet or below 1,500 feet (outside of the
phlebotomus zone).
71.1. Pinta (carate).—a. Etiologic agent.—Various fungi have been suspected
but since 1938 a spirochete, Treponema carateum, morphologically identical with
T. pallidum, has been accepted by some authorities as the causative agent. It
may be found in tissue juice from skin lesions and lymph nodes.
b. Geographical distribution.—Mexico, West Indies, Central America, and
South America.
c. Transmission.—The disease occurs in damp, low-lying tropical regions. It
affects the dark races chiefly and is rare in whites. It occurs most often in young
adults from 15 to 25. There is no proof of congenital transmission, and it is
apparently not contagious by person-to-person contact. Transmission may be
by the bite of a blood-sucking insect (perhaps by a species of Simulium in some
cases).
d. Recognition.—The initial lesion appears at the site of the port of entry
of infection as a minute papule which appears 7 to 10 days after inoculation.
Distribution of skin lesions is localized at outset; later the lesions may be
generalized. Eruption is often symmetrical, at times strikingly so. In extremely
rare cases it is unilateral. Location of the eruption is usually on face and extremities
; often over bony prominences, such as knuckles and malleoli. It may
affect any part of skin except the scalp. Palms, soles, and genitals are rarely
affected. Small patches may be present on mucous membranes. Color of skin
lesions is usually a shade of blue (slaty or leaden). Bluish color may be either
diffuse or stippled. When blue pigmentation eventually disappears there is left
a partial depigmentation which may go on to complete depigmentation, simulating
vitiligo. Course of disease is extremely chronic.
e. Specific diagnosis.—Demonstration of the causative agent in material from
typical lesions. According to Leon y Blanco, positive Wassermann reactions
were not obtained prior to the development of secondary lesions, and only in the
advanced cases with marked pigmentation did the positive tests approach 100
percent.
f. Treatment.—As for yaws. Optimum amount and duration of treatment is
not yet established.
g. Prevention.—Muss treatment of infected individuals. Avoidance of contact
with infective lesions. Precautions to avoid the bites of flies and gnats.
71.2. Plague.—a. Etiologic agent.—Pasteurella pestis.
b. Geographical distribution.—Endemic in India, Indo-China, the East Indies,
New Caledonia, Central China, Manchuria, and Mongolia. Less important foci of
endemic infection exist in Africa (Morocco, Egypt, Uganda, Angola, Kenya, Madagascar,
and the Belgian Congo), in South America (Brazil, Ecuador, Peru, Bolivia,
and Argentina), and in the Azores. Sporadic cases have occurred in almost
all the major seaports of the world, including those of the United States.
c. Transmission.— (1) Plague occurs as an epizootic disease among domestic
rats, and is transmitted from rat to rat and from rat to man by certain fleas
(Xenopsylla cheopis and others). Infection of man may occur by regurgitation
of P. pestis into the wound when the flea bites, or by inoculation of the infective
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feces of the flea. Plague in humans exists largely because of the domestic habits
of rats and its occurrence as an endemic or epidemic disease is largely conditioned
by the density of the rat population.
(2) In addition to flea-borne transmission, infection may result from handling
infected rodents or infectious tissues.
(3) It must also be remembered that human cases of plague may disseminate
the disease directly by droplet infection or by expectoration or by discharge from
buboes.
d. Recognition.—Incubation period is usually 3 to 7 days, occasionally longer.
Case fatality rate high. There are three chief clinical types: (1) Bubonic (most
common).—Characterized by enlargement of lymph nodes (buboes) draining the
area of the flea bite. There is usually a rapid and severe course, with high fever
and great prostration.
(2) Septicemic (less common).—May be generalized lymph node enlargement,
subcutaneous hemorrhages, and pustules. Course is rapid and overwhelming,
generally fatal.
(3) Pneumonic.—Clinical picture is that of a virulent septic pnuemonia;
fulminating course ; thin, mucoid, bloody sputum; almost invariably fatal. Plague
pneumonia may develop in bubonic cases, or from handling infected rodents or
by droplet infection from another case.
e. Specific diagnosis.— (1) Smear of aspirated bubo contents or sputum stained
with methylene blue shows short bacilli (Pasteurella pestis) with bipolar staining
and sometimes with swollen, vacuolated, involution forms.
(2) Culture from bubo, blood, or sputum on nutrient agar or in broth shows
characteristic Gram-negative organisms.
(3) Inoculation of bubo juice, blood, or sputum into mice, rats, or guinea pigs,
intraperitoneally, or by skin scarification, produces death in 24 to 72 hours. At
autopsy of animal, characteristic lesions are found and P. pestis can be recovered.
Warning: All infectious material must be handled with the greatest care.
All animals inoculated for plague diagnosis must be free of fleas and other
ectoparasites prior to inoculation and thereafter kept in insect-proof cages in a
separate room from other animals. All persons handling smears, cultures, cages,
or inoculated animals must wear gowns, rubber gloves, and masks, and must
observe the strictest aseptic technique.
f. Treatment.— (1) General.—Morphine as indicated for restlessness and
delirium. Force fluids by mouth or parenterally for toxemia.
(2) Chemotherapy.—Sulf a thiazole by mouth as follows: Initial dose 4.0 grams
(60 grains) ; subsequent doses 1.5 grams (22% grains) every 4 hours day and
night until temperature has been normal for 5 to 7 days. It should be borne in
mind that the toxic effects of these large doses may mask clinical improvement
in the disease. In fulminating cases intravenous sodium sulfathiazole (5 percent
solution in sterile distilled water) may be tried as follows: Initial dose, 0.06 gram
(1 grain) per kilo of body weight given slowly. Subsequent doses 0.03 gram per
kilo every 6 hours. Change to oral dosage as soon as possible. The use of
sulfadiazine in man has not been reported to date (December 1942), but in mice
it is more effective and less toxic than sulfathiazole.
(3) Surgical.—Hot, wet applications to the bubo may hasten localization of
the infection. Incision should be delayed until localization is complete in order
to avoid blood stream infection.
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g. Prevention.— (1) Isolation of patient.—This is imperative. Keep patient
in separate screened room and allow only attendants to enter. Burn all waste
articles contaminated by discharges. In pneumonic or suspected pneumonic cases,
attendants must wear hoods with goggles or plastic eye openings, coveralls or
complete gown with trousers, and rubber gloves. Sterilize all bedding, linens,
and utensils in contact with patient, by boiling or autoclaving. Wash walls and
floor of room and all furniture with 5 percent cresol compound after discharge
of case and allow room to air for 48 hours. Handle bodies of persons dying of
plague with strict antiseptic precautions.
(2) Sanitary measures.-—(a) Ratproof buildings and ships.
(6) Carry out rat extermination program by trapping and poisoning with red
squill, or by fumigation with methyl bromide or cyanide gas. Cyanide fumigation
should be performed* only by thoroughly trained personnel.
(c) Keep under constant surveillance the incidence of plague in the rat population
of port and other cities of the endemic areas. “Plague in rats usually precedes
plague in humans.”
(d) Constant vigilance should be exercised in and around camps to prevent
rodent harborages and access of rats and other wild rodents to food supplies,
special attention being given to the thorough collection and proper disposal of
garbage.
(e) If a bubonic case occurs, determine source of infection. If source is in a
city or town, trap and examine rats from focus of infection outward until no
more plague-infected rats are found. Then trap and poison from periphery of
infected area to center and follow at once with ratprooflng and destruction of
rat harborages.
(f) If a pneumonic case occurs, quarantine all contacts under guard, and
take temperatures every 12 hours for 7 days. Also quarantine under military
or police guard the area where the infection was acquired and where contacts
may have occurred, prohibit entrance and exit of inhabitants, and make houseto-
house inspection, taking temperatures twice daily until 7 days after last case
is discovered, isolating all persons developing fever regardless of cause. Guards
should be cautioned to avoid close contact with quarantined persons. Inspecting
personnel should wear gowns, coveralls, caps, masks, and rubber gloves. (See
AR 40-205 and 40-210.)
(3) Immunization.—All military personnel under serious threat of exposure to
epidemics of human plague should be immunized with plague vaccine. (See
AR 40-210 and sec. VII.) The initial vaccination consists of 2 subcutaneous
injections of plague vaccine with an interval of 7 to 10 days between injections.
The first dose is 0.5 cc and the second dose 1.0 cc of vaccine. Additional 1.0-cc
doses of plague vaccine may be administered whenever, in the opinion of the
surgeon, additional stimulation of immunity is necessary.
Ji. Sylvatic plague.— (1) General.—This is flea-borne plague, caused by P.
pestis. It occurs as an epizootic disease among wild rodents (ground squirrels,
marmots, rabbits, and others) which do not ordinarily live in close association
with man. This type of plague may be the source of sporadic human infections
and may be introduced into the domestic rat population of cities, following
which epidemics of rat plague and human plague may occur.
(2 ) Control measures.— (a) Avoid unnecessary contact with wild rodents.
(& ) In endemic rural areas control wild rodent population by shooting, poisoning,
gassing, and filling of burrows.
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71 .3. Relapsing fever—louse-borne.—a. Etiologic agent.—Variously designated
spirochaetes as, for example, Borrelia recurrentis or Spirochaeta obermeieri
in European relapsing fevers.
b. Geographical distribution.—This disease has a cosmopolitan distribution and
is likely to occur in epidemic form wherever lousiness prevails. Epidemics ■ in
the last. 25 years have occurred in eastern Europe, northern Asia, India, China,
western Asia, North Africa, and Equatorial Africa. Lesser outbreaks have been
reported from Peru, Central America, French Indo-China, and Japan. Chief foci
since 1934: Africa and Russia.
c. Transmission.—From man to man by Pediculous humanus (head and body
louse) and possibly by Phthirus pubis (crab louse). Crushing of louse by scratching
liberates the microorganisms which enter the body through abraded skin.
d. Recognition.—Onset is sudden with headache, generalized pains, chills, and
fever of 104° F. to 105° F. The temperature usually remains high 4 to 6 days
and then subsides abruptly by crisis. Vomiting, splenomegaly, leucocytosis, and
albuminuria may occur during the acute febrile stage. An afebrile period of
4 to 8 days is followed by a relapse with similar but milder symptoms. Several
relapses may occur unless treatment is instituted. Mortality varies from 2 to
50 percent.
e. Specific diagnosis.—Demonstration of Borrelia in the blood during febrile
periods by darkfield examination, by Giemsa-stained thin or thick films, or by
mouse inoculation with the blood of the patient, in which case the organism
appears in the blood of the mouse 24 to 48 hours later.
f. Treatment.—Inject 0.6 gram of neoarsphenamine intravenously. One dose
usually cures, but two or three doses may be necessary. This therapy is most
effective at beginning of the initial attack or of a relapse; it is dangerous at
the time of crisis or just after it, since the patient may collapse. Occasional cases
are resistant to this drug. Good nursing during the fever is important. Mapharsen
has been used in a few cases with good results and there is reason to believe
that it may replace neoarsphenamine. It should be used in doses of 0.04 to 0.06
gram intravenously.
g. Prevention.—Apply measures for eradication of lice (see louse-borne typhus).
No method of immunization has been developed.
71 .4. Relapsing- fever—tick-borne.—a. Etiologic agent.—Spirochaetes, variously
designated as Borrelia, Spirilla, Spirochaeta, Spironema, or Treponema,
with such so-called geographical strains as, for instance, Borrelia duttoni in the
relapsing fever of tropical Africa.
b. Geographical distribution.—Patchy distribution; does not tend to spread;
generally remains localized in areas corresponding to distribution of the tick
vector. It is a “place” or “house” disease. Foci in Africa, Asia, Europe, Canada,
United States (western and southwestern States), Central America, and South
America.
c. Transmission.—From lower animal reservoir hosts to man by soft ticks of
the genus Ornithodorus. The reservoir hosts include many kinds of rodents,
monkeys, possibly bats, and other mammals. The ticks are found in native huts
and in the burrows and nests of wild rodents. In the United States they may
be found in the cabins and cottages of the western recreational areas and in
the caves of the Colorado River Valley. In human habitations they have the
feeding habits of bedbugs. Attachment to host for feeding is usually brief (12
to 15 minutes) but may continue for 1 hour.
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d. Recognition.—Clinically similar to the louse-borne type except that—
(1) Cerebro-spinal symptoms are more common in some areas.
(2) Paroxysms are more intense but of shorter duration, 2 to 4 days.
(3) Greater number of relapses occur, usually more than four.
(4) Mortality is lower (average 5 percent).
e. Specific diagnosis.—Same as for the louse-borne type.
f. Treatment.—Same as for the louse-borne type. Some workers report that
tick-borne relapsing fever in certain areas is very resistant to arsenicals.
g. Prevention.— (1) Avoid sleeping in native huts and cabins in endemic areas.
(2) Avoid caves inhabited by rodents, bats, or ticks.
(3) Avoid soiling hands with blood of rodents in endemic areas.
(4) In endemic regions, sleeping quarters should be so constructed as to
discourage entrance or nesting of rodents beneath floors or in walls and the
harborage of ticks in cracks in floors or walls.
(5) Cleanliness of barracks, tents, and other quarters should be maintained,
to prevent the accumulation of dust and debris which might give harborage to
ticks and other vermin.
(6) Instruct personnel to examine day and night clothing and bedding for
ticks after possible exposure.
71.5. Rickettsial diseases—classification.—The rickettsial diseases discussed
in the following pages are epidemic and endemic typhus, Rocky Mountain spotted
fever, tsutsugamushi disease, and “Q” and trench fevers. These may be outlined
as follows:
Typhus fevers
Tick-borne spotted fevers________
Mite-borne fever________________
Miscellaneous group____________ ■
Epidemic louse-borne.
Endemic flea-borne.
Rocky Mountain spotted fever__
Exanthematic Brazilian typhus _
Fievre boutonneuse________________
kS. African tick-bite fever_________
Tsutsugamushi fever (Japan,
China, Malaya, and Sumatra).
Tick-borne “Q” fever in Australia.
Louse-borne trench fever of the
, first World War.
No
primary
sore.
Primary
sore.
71.6. Epidemic typhus (louse-borne or European typhus).—a. Etiologic
agent.—Rickettsia prowazeki.
b. Geographical distribution.—Chiefly in Europe, North Africa, Asia, and in the
higher altitudes of Central and South America. Not present in the United States
or insular possessions.
c. Transmission.—The reservoir of the disease is man. Transmission is from
man to man by the louse, Pediculus humanus. It is chiefly a disease of winter
and spring, and affects especially impoverished, overcrowded, and dirty peoples.
d. Recognition.—Incubation period 6 to 14 days. Onset usually sudden, with
chills, fever, general pains, and severe headache. The fever continues for about
2 weeks. A macular papular eruption appears on the fourth to the sixth day which
may become petechial. Typically the rash appears first on chest or abdomen,
spreads to back, arms, legs, and rarely in severe cases, to palms, soles, and face.
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Mental dullness is common, especially during the second week. Case fatality
rate 20 to 60 percent. One attack confers immunity which is not always permanent.
e. Specific diagnosis.—Agglutination of B. proteus 0X19 (Weil-Felix agglutination)
occurs during the febrile period of the disease, increases in titer during early
convalescence, and disappears in late convalescence. The reaction is of diagnostic
importance when a rising titer occurs. Single tests are of little diagnostic value,
and a differentiation between typhus and Rocky Mountain spotted fever cannot be
made by this test alone. It is important to use to “O” or nonmotile variant B.
proteus. Of great importance is specific rickettsial complement fixation. This
test becomes positive about the eighth day and increases in titer, remaining positive
for years after the attack. By employing specific antigens, epidemic and endemic
typhus may be distinguished. The complement fixation test is performed routinely
at the Army Medical School, Washington, D. C. Guinea pigs inoculated with
infective blood develop a characteristic temperature curve after a period of incubation.
One attack confers an immunity to a second inoculation.
f. Treatment.—Symptomatic. Absolute rest in bed, with good nursing care.
Maintenance of fluids by mouth, rectum, or hypodermoclysis. Relief of constipation
by means of enemas or mild laxatives. Tepid sponges for lowering fever.
Relief of headache by aspirin or codeine; morphine may be necessary. No
specific treatment of proven value has been developed. A hyperimmune rabbit
serum is under study, but is not yet generally available. The sulfonamide drugs
have been tried without benefit.
g. Prevention (see AR 40-205, 40-210, and 615-250).— (1) Delousing clothing.—
(a) Methyl bromide.—Recent studies indicate that the best delousing of clothing
and equipment can be obtained by the use of QM issue methyl bromide, either in
portable and demountable forced air circulation gas chambers made of plywood,
or in special QM issue bags made impervious by impregnation with ethyl cellulose.
Clothing and equipment are not injured by this method. The fumigant,
methyl bromide, is slightly more toxic than carbon tetrachloride, but when used
in the prescribed manner it can be safely handled and gas masks are not required
by the personnel involved. The gas has great powers of penetration and when
the proper dosage is used it will, in 30 minutes, destroy all insects or insect eggs,
even if they are on clothing in the center of a filled barracks bag. Clothing fumigated
in this way can be safely reissued to the owners within 1 hour, or by the
time the concurrent body delousing and bathing procedures have been finished.
(&) Steam.—Very efficient. Suitable apparatus may easily be improvised.
Causes shrinkage of woolen goods and wrinkling of clothing; damages leather,
felt, and webbing. Pressure sterilizers are employed to best advantage in permanent
delousing stations; emergency stations may employ a method utilizing flowing
steam, such as the Serbian barrel.
(c) Dry heat.—135° F. for 5 minutes. Does not injure leather, metal, or webbing,
and does not wrinkle clothing. Difficult to secure penetration of dry heat
into clothing.
(d) Hot water.—Is not suitable as it causes shrinkage of woolen goods and
damages felt and webbing.
(e) Insecticidal powder.—The approved QM issue insecticidal powder may be
dusted into the seams of clothing every 7 to 10 days, not only as a delousing
measure but as a prophylactic against infestation.
(2) Delousing persons.— (a) The delousing of the body surface may be accomplished
by clipping or shaving of the hair and the application of vinegar or 15
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percent acetic acid to loosen eggs. Then shampoo vigorously with hot soapy
water containing 25 percent kerosene and remove any retained nits or eggs by
combing with a fine comb.
(&) When available, the following insecticidal preparation may be used:
Pyrethrins________________________________________________________________ 2.5
IN 930________ 20
Castor oil___________________________________________________ ;_____________ 20
Isopropyl alcohol-------------------------------------------------------------- 810
Water, q. s. ad______________________ _____________________________________1,000
Apply to hairy parts 15 minutes before bathing.
(c) Another satisfactory method of destroying head and crab lice is to apply
8 cc of one of the following insecticide solutions 24 to 48 hours prior to delousing
of clothing and bathing:
Lethane 384 special_______________________________________________________500
Mineral oil__________________________________________________________________ 500
or
Lauryl thiocyanate:_________________________________________________________250
Mineral oil___________________________________________________________________ 750
(d) In the absence of these special preparations, dust the hairy parts of the
body liberally with QM issue insecticidal powder and rub in. Follow in 24 to
48 hours by soapy bath and combing out of retained nits.
(3) Control patients.—All patients and contacts should be carefully
deloused. This includes destruction of lice and eggs in the clothing as well as
on the body. Contacts should be revaccinated with typhus vaccine unless so
vaccinated within 2 months. The clothing of typhus patients should be steam
sterilized to destroy all infective materials.
(4) Vaccination.—A vaccine prepared with killed rickettsiae has been provided.
At present this vaccine is administered by giving three injections, of
1 cc each, subcutaneously, at approximately weekly intervals. A stimulating
dose of 1 cc should be administered every 4 to 6 months as long as serious danger
of infection exists. Additional injections may be given whenever, in the
opinion of the surgeon, additional stimulation of immunity is deemed advisable.
For further details see section VII.
71.7. Endemic typhus (murine or flea-borne typhus).—a. Etiologic agent.—
Rickettsia mooseri.
b. Geographical distribution.—Endemic typhus has been found in all regions
where the epidemic disease occurs. However, endemic typhus may occur alone,
as it does in the southern part of the United States.
c. Transmission.—The reservoir .of the disease is in rats and the disease is
transmitted to man by rat fleas, particularly Xenopsylla cheopsis. The disease
apparently is transmissible from man to man by the body louse. Epidemics
of murine typhus may thus occur in a lousy population although the disease is
not ordinarily associated with lousiness or poverty. Endemic typhus occurs
chiefly in late summer and fall in persons having contact with rats, or living
or working on premises harboring rats, especially grocery stores, food or grain
warehouses, or restaurants.
d. Recognition.—Incubation period 6 to 14 days. Clinically similar to epidemic
typhus, except that the course is milder and the rash may be less profuse and
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of shorter duration. Case fatality rate about 5 percent. The chief differential
diagnosis is from Rocky Mountain spotted fever.
e. Specific diagnosis.—Weil-Felix agglutination 0X19 same as for epidemic
typhus. Specific rickettsial complement fixation tests are of great assistance
in differentiating endemic from epidemic typhus, as indicated above. Guinea
pigs inoculated with infected blood develop a characteristic temperature curve
after a period of incubation. In the guinea pig this disease is usually characterized
by scrotal swelling and the appearance of “Neill-Mooser bodies” in scrapings
from the inflamed tunica vaginalis. “Neill-Mooser bodies” are enlarged
serosal cells filled with intracytoplasmic rickettsiae. Rocky Mountain spotted
fever is differentiated as follows :
Endemic typhus Rocky Mountain spotted fever
History_______________ _______
Fever________________________
Rash_________________________
Pulse_________________________
Leucocytes______ \_____________
Weil-Felix (0X19)_____________
Complement fixation___________
Exposure to rat fleas___________
Two weeks___ ______ _________
First on body; spreads to extremities.
Palms and soles usually free_____
Neck and face rarely involved___
Usually fades before defervescence-
100 or less_____________________
Normal limits_________________ _
Second week__________________
Positive with typhus antigen____
Exposure to ticks.
Three weeks.
First on extremities; spreads to
body.
Palms and soles usually affected.
Neck and face commonly involved.
Usually persists until defervescence.
100 to 130.
10,000 to 18,000.
Second or third week.
Positive with spotted fever
antigen.
f. Treatment.—Same as for epidemic typhus.
g. Prevention.— (1) Elimination of rats by ratproofing, trapping, and poisoning.
Special care should be directed to proper protection and disposal of garbage to
prevent access by rats. (See AR 40-205 and 40-210.)
(2) The isolation of patients is not necessary in the absence of body lice.
(3) Vaccination.—The incidence of the disease is too low to warrant general
vaccination. This procedure is not considered in places where the rat population
can be controlled.
71.8. Rocky Mountain spotted fever (tick fever, exanthematous tick fever,
tick typhus, Brazilian spotted fever (Sao Paulo typhus)).—Immunologically
related diseases: Boutonneuse fever (Mediterranean littoral), Kenya typhus
(East Africa), Tobia fever (Colombia), and South African tickbite fever.
a. Etiologic agent.—Rickettsia rickettsii (Dermacentroxenus rickettsi).
b. Geographical distribution.—Reported from nearly all States of the Union,
Also present in British Columbia and Alberta and in Brazil and Colombia. About
1,000 cases are recognized annually in the United States.
c. Transmission.—Reservoir hosts probably some species of rodents or other
animals. Wood ticks (Dermacentor andersoni) in the western States and dog
ticks (Dermacentor variabilis) in the eastern States transmit the disease to man
during the process of feeding. Other species of ticks are the vectors in other
countries. Seasonal occurrence in northwestern States principally during spring
and early summer; in the eastern and southern States throughout the summer.
Rarely cases occur as late as December.
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d. Recognition.—There is usually a history of exposure to tick bite. Incubation
period 2 to 14 days, usually about 1 week. General features like those of
epidemic typhus, but usually more severe. Duration of fever usually about 3
weeks. Defervescence usually by rapid lysis. Meningismus is not uncommon.
Delirium, convulsions, and coma may develop in severe cases. There is usually a
leucocytosis of 10,000 to 18,000. Eruption similar to typhus but more intense
and usually becomes purpuric. Appears first about wrists and ankles, rapidly
spreads over body, but less intense on trunk. Usually involves palms and soles.
Persists until defervescence. Rash is followed by brownish stain and often by
desquamation. Case fatality rate about 25 percent.
e. Specific diagnosis.—Weil-Felix agglutination OX19 is similar to that described
for epidemic typhus. A specific rickettsial complement fixation reaction
may be obtained beginning usually about the tenth day and remaining positive
for years after convalescence. By means of this test Rocky Mountain spotted
fever can be distinguished from either epidemic or endemic typhus.
f. Treatment.—Same as for typhus. A hyperimmune rabbit serum has recently
been developed. It is only of value when administered during the early stages of
the disease.
g. Prevention.—Adult ticks are active from February through August. There
is some variation with the climatic conditions and the section of the country.
The disease is transmitted solely through tick contact. In order that the tick
bite may transmit the disease, the tick must remain attached for several hours.
(1) Tick control.— (a) Avoid tick infested area if possible. Common sites for
ticks: tall grass, especially along animal runs, bushes, along the edge of wooded
areas, and along streams.
(&) Remove ticks from clothing and body at least once a day, best done immediately
after coming from areas where ticks may be present and as a routine measure
on retiring. Ticks are likely to attach to the skin on the hairy portions of the
body or where their progress is stopped by constricting clothing, such as the belt.
Ticks should be removed gently to avoid breaking off the mouth parts. This can
be done with tweezers or with cotton saturated with iodine. The tick should
not be crushed with the bare fingers. Paint the site of the tick bite with tincture
of iodine. Wash hands thoroughly after handling ticks, especialy after removing
engorged ticks from animals. Dogs should be deticked at frequent intervals.
(2) Vaccination.—Vaccine is prepared at the Rocky Mountain Laboratory,
U. S. Public Health Service, Hamilton, Montana. It may be procured from that
laboratory or from the National Institute, of Health, Bethesda, Maryland, when
authorized by The Surgeon General. Limited amounts may also be obtained from
State health officers. The vaccine may be given in two or three doses of 1 or 2 cc
each, 1 week apart. Immunity is not absolute, but is apparently sufficient to
protect against death should spotted fever be acquired within a year subsequent
to vaccination. The vaccine is probably of no value after an infecting tick contact.
It is valueless in treatment. As a relatively small number of cases occur each
year, mass vaccination is not recommended in the Army.
71.9. Tsutsugamushi disease (Japanese river fever).—a. Etiologic agent.—•
Rickettsia orientalis (R. tsutsugamushi, R. nipponica).
b. Geographical distribution.—Japan, Formosa, Indo-China, Malaya, and prob,
ably India, Korea, Sumatra, the Philippine Islands, and Australia (Queensland).
c. Transmission.—The disease occurs in Japan in summer and fall months in
low-lying sections that are subject to river floods. Field mice are reservoir
hosts. The infection is transmitted to man in Japan by the larval form of the
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mite, Trombicula akamushi, and by other, species of mites elsewhere. The infection
is transmitted to the next generation of mites through the egg.
d. Recognition.—Incubation period is about 1 week. The fever lasts from 2
to 3 weeks. A macular papular rash appears on the second to seventh day,
first on trunk and arms, and rapidly becomes generalized. There is usually a
local ulcer at the site of the infecting bite and the regional lymph nodes become
enlarged and tender. Later there may be a general lymph node involvement.
Leucopenia is usually present.
e. Specific diagnosis.—Agglutinins for B. proteus OXK occur but not for 0X19.
Case fatality rate 40 to 55 percent in Japan, 4 percent in Sumatra. Immunity
is confered by an attack, although second attacks have been noted.
f. Treatment.—Same as for typhus.
g. Prevention.—Avoid unnecessary exposure in infected areas during summer
and fall. Bathing in hot water with soap immediately after exposure and
change of clothing may prevent infection. Insect repellents such as dimethylthallate,
QM issue insecticide powder, or equal parts of flowers of sulfur and talcum
powder, may be of value. No vaccine against the disease has been developed.
71.10. “Q” fever.—a. Etiologic agent.—Rickettsia burneti (R. diaporica).
b. Geographical distribution.—Recognized as a natural infection in humans
in Australia. Cases in Washington, D. C., were probably laboratory infections.
The disease may be occurring unrecognized in other regions. Specific antibodies
in human blood have been demonstrated in Idaho, Montana, Wyoming, Nebraska,
Nevada, Arizona, and Washington State. In Montana the tick Dermacentor
andersoni has been found naturally infected.
c. Transmission.—Australian cases associated with handling of livestock. The
bandicoot, a marsupial, is apparently a reservoir host. Transmission to a man
by a tick Hemaphysalis humerosa has been suggested. Two types of the disease
may exist, one transmitted by a tick, the other through the respiratory tract, possibly
by dust containing the dried excreta of infected animals or anthropods.
d. Recognition.—Incubation period in the Australian cases is thought to be
10 days to 1 month. Onset acute, with fever, prostration, and headache, accompanied
by chills and sweats. Duration of acute stage from a few days to 3 weeks.
White blood cells are within normal limits. There is no rash. In most of the
laboratory cases in Washington, vague chest pains, unproductive cough, and rales
were present. X-ray examination of the chest showed a soft infiltrative lesion
which began centrally and spread outward. Clinically these cases could not be
differentiated from the atypical pneumonias reported frequently during the past
few years. Convalescence may be prolonged. The fatality rate is low.
e. Specific diagnosis.—Agglutinins are not produced for any of the strains of
Proteus X so far employed. In the second week complement-fixing antibodies
against R. burneti appear in the blood serum. The organism can be isolated in
guinea pigs by inoculation of blood taken during the febrile period, and protective
antibodies can be demonstrated in recovered cases.
f. Treatment.—Symptomatic. None of the sulfonamide compounds has been
found to be of any benefit.
g. Prevention.—Further knowledge is required before control measures can be
evolved.
71.11. Trench fever (Wolhynian fever, 5-day fever).—a. Probable etiologic
agent.—Rickettsia quintana.
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b. Geographical distribution.—Trench fever appeared during the first World
War. It became epidemic in nearly all the armies of Europe and later spread to
Mesopotamia. Only a few cases have been recognized since the last war.
c. Transmission.—-As demonstrated by human experiments, the infection may
be transmitted by the body louse. Recovered cases of trench fever may remain
infective to lice for months. The virus in the dried louse excreta remains virulent
for at least 4 months. It also retains its virulence in the dried urine of patients.
The disease has never been transmitted to laboratory animals. The infecting
agent is present in the blood of human cases, as has been shown by injecting the
patient’s blood into voluteers, but rickettsia have not been demonstrated in humans.
d. Recognition.—Incubation period 1 to 3 weeks. Onset sudden, with prostration,
and severe pain in the muscles and bones, particularly the tibia-, radius, and
ulna. Frontal headache and ocular pains may be severe. Congestion of the conjunctivae
is common. The spleen is generally enlarged. In the majority of
cases a rash develops on the first or second day of fever, consisting of small
macules mainly on the trunk. It does not become petechial. Sweats are common.
The leucocyte count is usually between 10,000 and 12,000. The initial bout of
fever lasts about 5 days. Relapses occur at intervals of 5 to 6 days or even
longer. Three to five relapses may occur. Prostration is pronounced and convalescence
prolonged. The disease is not fatal. Immunity is apparently not
established by one attack.
e. Specific diagnosis.—None. The reaction of the serum to the Weil-Felix agglutination
test is not known.
f. Treatment.—Entirely symptomatic.
g. Prevention.—Delousing (see epidemic typhus). The virus is present in the
urine and saliva of patients. Therefore, attendants should be protected against
contact infection, body discharges should be disinfected, and clothing and bedding
should be disinfected with steam or by disinfectant solution, such as cresol, 2 to
3 percent. (See AR 40-205 and 40-210.)
71.12. Schistosomiasis.—There are three schistosomes (blood flukes) which
cause serious diseases in man.
a. Schistosoma haemtobium, producing mainly genito-urinary symptoms.
b. Schistosoma mansoni, producing mainly intestinal symptoms.
c. Schistosoma japonicum, producing mainly hepatic symptoms.
71.13. Schistosomiasis produced by S. haematobium (Bilharziasis, endemic
haematuria).—a. Geographical distribution.—Especially prevalent in the Nile
Valley; also in other areas of Africa and in parts of Asia and Europe bordering
on the Mediterranean.
b. Transmission.—The adult worms live and lay their eggs in the veins around
the bladder. The eggs escape in the urine, rarely in the feces. When deposited
in fresh water, the egg hatches and the embryo (miracidium) enters a snail
(genus Bulinus, Physopsis, and others). The snails may be found in fresh water
with slightly alkaline reaction, usually containing aquatic vegetation, and occasionally
in brackish water. They may inhabit slow-moving streams, irrigation
ditches, limestone sinks, reservoirs, and small pools after flooding of streams.
Larvae (cercariae) emerge from the infected snails and enter the water, infecting
man or animals by penetration of the skin. Thus the disease may be contracted
while bathing, wading, working, or washing clothes in infected water, or by
drinking such water and possibly through the use of a polluted public water
supply.
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c. Recognition.— (1) Early.—Papular dermatitis at site of penetration of the
cercariae.
(2) Four to eight weeks after infection.—Fever, giant urticaria, eosinophilia,
and hematuria.
(3) Late.—Vesical ulcers, urinary calculus, and papillomata, urinary flstulae,
splenomegaly, and cirrhosis of liver.
d. Specific diagnosis.—Presence of characteristic terminal-spined ova in urine,
rarely in feces.
e. Treatment.— (1) Fuadin (neoantimosan) intramuscularly; 1.5 cc, 3.5 cc, and
5.0 cc on successive days, then 5.0 cc on alternate days to a total of 10 doses.
Toxic symptoms: vomiting, joint pains (rare). If toxic symptoms appear, reduce
dosage. If eggs containing living embryos are found after completion of treatment,
repeat treatment after a rest of 1 week. (See (2) below.)
(2) If a satisfactory response is not attained with these courses of fuadin, use
potassium antimony tartrate (USP), 2 percent freshly prepared solution intravenously
on alternate days. Initial dose 2.5 cc (0.05 gram) ; increase each subsequent
dose by 1.25 cc until 7.5 cc are being given; continue until a total of 12
to 15 doses have been given. Administer 2 to 3 hours after a light meal and
have patient lie down for 1 hour after administration. If toxic symptoms appear,
reduce dosage.
(a) Toxic symptoms.—Coughing immediately after administration (not important)
; nausea, vomiting, dizziness, and collapse.
(&) Contraindications to antimony preparations.—Nephrities, jaundice, or
severe liver disease.
(3) Diet.—The diet should liberally supply all the essential nutrient substances.
If evidence of hepatic disease exists, the diet should be high in carbohydrates and
low in fats. Milk, eggs, and cheese are permissible. The supplementation of the
diet with vitamin A and vitamin B complex is advised.
(4) Criterion of cure.-—Cessation of passage of eggs containing live embryos.
If cure is not obtained, repeat treatment after 1 month.
f. Prevention.— (1) Avoid entering or using unpurifled fresh water in endemic
areas. The apparent absence of snails from such water does not guarantee that
the water does not contain cercariae.
(2) In case of accidental or unavoidable entrance into water containing cercariae,
immediate and complete bathing with soap and pure water may prevent
infection.
(3) If it is necessary to provide bathing facilities in a natural body of fresh
water in an endemic area, a preliminary survey of the surrounding population
should be made to exclude the presence of schistosomiasis. Steep banks and wave
action diminish the probability of the presence of snails. Copper sulfate in a dilution
of 1/200,000 will kill cercariae and snails.
71.14 . Schistosomiasis produced by S. mansoni (intestinal schistosomiasis).—
a. Geographical distribution.—In the Nile Valley and in many other parts of
Africa, coexisting with £?. haematobium; also in South America (Brazil, Dutch
Guiana, and Venezuela) and West Indies (Puerto Rico, Vieques, the Lesser Antilles,
including St. Lucia, Antigua, St. Kitts, Nevis, Montserrat, Martinique,
Guadeloupe, and St. Martin).
b. Transmission.—The adult worms live and lay their eggs in the veins around
the colon and rectum. The eggs are discharged in the feces, rarely in the urine;
some are carried to the liver. Otherwise the life cycle closely resembles that of
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& haematobium except that the snail hosts belong to the genera Planorbis or
Australorbis.
c. Recognition.—Same as in <8. haematobium infections except that the colon
and rectum, instead of the bladder, are the principal organs involved, and the
late clinical findings are bloody stools, rectal polyps and fistulae, and prolapse of
the rectum. Hepatic cirrhosis and splenomegaly are more pronounced than in
R haematobium infections.
d. Specific diagnosis.—Presence of characteristic lateral-spined ova in feces,
rarely in urine.
e. Treatment and prevention.—Essentially the same as for 8. haematobium
infection.
71.15 . Schistosomiasis produced by S. japonicum (oriental schistosomiasis,
Katayama disease).
a. Geographical distribution.—Occurs only in the Far East. Common in China,
particularly in the Yangtse Valley, also along China Coast from Shanghai to
Canton, and in Yunnan Province. Less common in Japan, Formosa, and the
Philippines (Leyte and Samar Islands) ; possibly in Celebes and Shan States
of Burma.
b. Transmission.—The adult worms live and lay their eggs in the veins of the
small intestines. The eggs are discharged in the feces; many are carried to
the liver. Otherwise the life cycle closely resembles that of 8. haematobium
except that the snail hosts belong to the genera Oncomelania and Katayama.
c. Recognition.—Same as in & mansoni infections except that rectal and anal
lesions are less common, while hepatic cirrhosis and splenomegaly are very common
and are the essential late symptoms.
d. Specific diagnosis.—Presence of characteristic spineless ova (rudimentary
lateral spines sometimes discernible) in feces, not in urine.
e. Treatment and prevention.—Essentially the same as S. haematobium.
71.16 . African trypanosomiasis (sleeping sickness).—a. Etiologic agent.—
Trypanosoma gambiense and Trypanosoma rhodesiense.
b. Geographical distribution.—Endemic throughout most of tropical Africa, the
boundaries roughly extending from Senegal east to Bahr el Ghazal Province
of the Southern Sudan, thence south through the lake country of East Africa
into Portuguese East Africa and thence west to Angola.
c. Transmission.—The trypanosomes are blood parasites of man and some
wild domestic animals which may serve as reservoir hosts, transmitted by various
species of tsetse flies of the genus Glossina, especially G. palpalis, G. tachinoides,
G. morsitans, and G. swynnertoni. Under favorable conditions the fly becomes
infective in from 18 to 34 days after ingestion of infected blood. Man is infected
by the introduction of trypanosomes by the bite of the infected tsetse fly. These
flies bite only in daylight. Under epidemic conditions simple mechanical transmission
by other biting flies and insects may possibly occur.
d. Recognition.— (1) Bite of an infected fly often produces more local reaction
than that of an uninfected fly. After an incubation period usually varying from
10 days to 3 weeks, irregular remittent fever, rapid pulse, deep hyperesthesia
and asthenia appear, often accompanied by headache and neuralgic pains. Delirium
and acute fever may occur early in T. rhodesiense infections. In white
individuals a characteristic erythematous skin rash on the trunk or thighs is
common. The individual lesions are round or oval patches, pinkish in color
with a clear center. Pruritus and dryness of the skin are common. The liver
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and spleen may be enlarged and the Wassermann reaction may be positive.
Enlarged lymph glands, especially those of the posterior triangle of the neck,
are an important diagnostic sign. Glands are discrete, at first soft and elastic,
later shrinking and becoming fibrotic. Enlargement persists usually from the
second to the sixth month of the disease.
(2) The cerebral stage (sleeping sickness) may be ushered in by tremor of
tongue and fingers, headache, delusions, hysteria, mania, and the other signs
of meningo-encephalitis and meningo-myelitis. Somnolence is the characteristic
cerebral symptom. Late cases show marked wasting from starvation.
e. Specific diagnosis.—Early diagnosis depends upon demonstration of trypanosomes
in lymph nodes, blood, or spinal fluid. Aspiration of fluid from lymph
node puncture with hypodermic needle and syringe is most likely to reveal
trypanosomes. Fresh unstained coverslip preparations reveal organisms by their
active movement even if they are few in number. Check with smear stained
with Wright’s stain. Blood smears are less useful but may show trypanosomes
in fresh coverslip preparations, thin stained smears, or better in thick blood
drop preparations as for malaria. Centrifuged citrated blood may reveal light
infections. Spinal fluid should be examined in all early cases for increased cell
count and globulin, and should be centrifuged for trypanosomes as evidence of
cerebral involvement.
f. Treatment.—All cases should be treated in a well-screened hospital.
(1) Early cases.—(a) Tryparsamide, dissolved in 10 cc of distilled water
(salt solution must not be used) : 15 weekly intravenous injections. Individual
dose 0.04 to 0.05 gram per kilo of body weight. Initial adult dose 1.0 to
1.5 grams, subsequent doses 2.0 to 3.0 grams. Vigorous complete treatment is
essential to avoid production of arsenic-fast strain. Toxic effect: Danger of
tryparsamide is optic atrophy. If photophobia, lacrimation, ocular pain, or
dimness of vision occur, reduce dose and lengthen interval to 10 days.
(&) Naphuride, Winthrop (Bayer 205, antrypol) intravenously in 10 cc of
distilled water every 4 days for four to six doses. Initial adult dose 0.3 to 0.5
gram, subsequent doses 1.0 gram. Toxic effect: Naphuride is a kidney irritant.
Urine should be free from albumin before treatment and must be examined after
each treatment and the drug discontinued if increasing albuminuria occurs.
(c) Lumbar puncture should be performed before and after completion of
therapy in every case, and every case should be kept under observation for at
least 2 years. Centrifuged citrated blood should be examined at completion of
therapy, monthly for the next 3 months, and then every 6 months for at least
2 years.
(2) Late cases.—Tryparsamide is the only drug of value in the treatment of
cases with involvement of the central nervous system. Dosage same as for
early cases. The drug should not be given intrathecally. Initial dose should be
half the standard dose because of dangers analogous to those in arsenical treatment
of cerebro-spinal syphilis. The spinal fluid affords a guide to the efficacy
of the treatment. First course of treatment should be 20 weekly injections. Repeat
course of treatment after interval of 1 to 3 months. The blood should be
examined periodically as previously indicated. The spinal fluid should be examined
before and after the second course of treatment and again 6 months and 1
year later. Late cases should be followed for at least 3 years.
g. Prevention.— (1) Control and examination of fixed personnel, especially
natives, in vicinity of station. Infected personnel should be held and adequately
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treated before being permitted to enter another area where tsetse flies are
present.
(2) Protective clothing.—The tsetse fly frequently bites on the legs; high
shoes with leggings or mosquito boots should be worn. Shorts should not be
worn.
(3) Gamp siting.—Camps should be located on high ground away from native
villages, streams, and forests. Buildings should be screened. Brush along
streams near stations should be cleared for a distance of 50 yards from the
water’s edge. Brush about camps should be cleared for a distance of 100 yards.
Motor vehicles should be inspected for presence of tsetse flies. Fishing and
hunting are dangerous in endemic areas.
71.17 . American trypanosomiasis (Chagas’ disease).—a. Etiologic agent.—
Trypanosoma cruzi.
b. Geographical distribution.—Brazil, Argentina, Uruguay, Venezuela, Peru,
Panama, San Salvador, Guatemala, and Mexico. Present in certain wild rodents
in California and in reduviid bugs in California, Arizona, New Mexico, and
Texas.
c. Transmission.—From man to man, and from animal reservoir (armadillo,
opossum, and certain rodents) to man by contamination of bite of cone-nosed
reduviid bug, especially Triatoma megista and T. infestans by feces of the
infected insect. These bugs habitually defecate while feeding and thus contaminate
the bite with their feces in which may be present the infective trypanosome.
d. Recognition.—A relatively uncommon disease occurring particularly in children
and characterized by invasion and destruction of the endothelial and other
cells, notably cardiac and striated muscle, by the Leishmania form of the parasite.
The acute stage is characterized by fever, facial edema, adenitis, and
anemia. Symptoms of the chronic stage depend upon the localization of the
parasite especially in the heart, central nervous system, thyroid, or suprarenal
glands. Pathogenicity for adults doubtful.
e. Specific diagnosis.—Diagnosis is based upon demonstration of the trypanosome
form T. cruzi in blood or the Leishmania form in the tissues, or demonstration
of the trypanosome in animals (guinea pigs) inoculated with patient’s
blood.
f. Treatment.—Symptomatic.
g. Prevention.—Avoidance of adobe and thatched huts of natives, where
Triatoma commonly hides.
71.18 . Typhoid fever.—a. Etiologic agent.—Bacterium typhosum (Eberthella
typhosa).
b. Geographical distribution.—World-wide. (The indigenous races of India,
Africa, and elsewhere are not immune.)
c. Transmission.—Typhoid fever is spread principally by food and water contaminated
by urine or feces of patients and carriers. Flies, fingers, or fomites
may convey infective material.
d. Recognition.—The incubation period varies from 8 to 14 days, usually 10.
The recognition of typhoid fever in the Tropics, where malaria and the dysenteries
are complicating factors, and particularly its recognition in individuals
who have been vaccinated, is not always easy. Clinically there may be the
typical constant or remittent fever with slow pulse, enlarged spleen, “rose” spots,
tympanites, muttering delirium, and leucopenia. Constipation rather than
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diarrhea is the rule in tropical typhoid. The rash is often absent or difficult to
differentiate from the many minor infectious and other skin lesions always
present in hot climates. In patients with malaria the onset of typhoid may
be abrupt with a rigor. The temperature usually becomes continuous but
may deviate from that typical of typhoid.
e. Complications.—The usual complications of intestinal perforation and hemorrhage
must be kept in mind. Perforation calls for immediate surgical intervention.
Localized purulent foci of infection may develop in gall bladder, bone
marrow, periosteum, or cartilage, and these also require surgical treatment.
Bed sores, phlebitis, myocarditis, and pneumonia may be complications. In
tropical areas the attack is generally more severe and more prolonged than
in temperate zones. Death may occur as early as the sixth day.
/. Specific diagnosis.—The only certain test, in previously vaccinated individuals,
is the isolation of B. typhosum in cultures. Blood culture is usually positive
during the first week or 10 days, sometimes longer, and sometimes during a
relapse. After 2 weeks of fever, positive cultures are more likely to be obtained
from feces and, less often, from urine. It must be remembered that a typhoid
carrier in the Tropics may be suffering from malaria fever although his stool or
urine gives a positive culture for typhoid. Blood serum agglutination test
(Widal reaction) usually becomes positive, 1 to 160 or more, during the second
week and usually remains positive through convalescence or longer. In previously
vaccinated persons positive tests are not a certain indication of typhoid
fever unless a rising titer can be demonstrated.
g. Treatment. —(1) Specific.—There is no specific chemotherapy or serum
treatment. In a few cases good results have been reported with sulfaguanadine
3.0 grams (45 grains) three times a day. But caution is indicated because of
the danger that the usual leucopenia of typhoid fever may develop under sulfa
drug therapy into an agranulocytosis. There is not yet sufficient evidence as to
the efficacy of chemotherapy.
(2) General.—Complete rest in bed until convalescence is well established.
Patients should be moved as little as possible. Careful nursing is most important.
Mouth must be kept clean. Purgatives should be avoided, using enemas
instead. Hot stupes to abdomen and use of rectal tube may relieve tympanites.
Alcohol rubs three or four times a day with tepid sponge baths should be given,
especially when the temperature is above 104° F.
(3) Diet.—Food should be given frequently in small amounts, totaling 3,000 to
4,000 calories per day, consisting of liquids and soft foods with little residue.
Milk, cream, butter, eggs, soft cereals, gelatin, and pureed cooked vegetables and
fruits, especially orange juice, can form the basis of the diet. They should be
fortified with carbohydrates, particularly lactose, with satisfactory provision for
vitamins of the vitamin B complex. This vitamin provision should include at least
3 milligrams of thiamin, 4.5 milligrams of riboflavin, and 30 milligrams of nicotinic
acid amide. Three of the standard multivitamin capsules daily will supply
these amounts. For the balance of the vitamins of the vitamin B complex, administration
daily of 3 cc of crude liver extract is suggested. Fluid intake should be
3,000 cc or more per day.
h. Prevention.— (1) Water and milk supplies must be carefully supervised, as
prescribed in AR 40-205. Only pasteurized or sterilized milk should be used. All
milk products must be protected after preparation from contamination by flies
or carriers.
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(2) Other foods must be protected from flies and carriers during and after
preparation. Raw vegetables and unpeelable fruits should not be served in the
Tropics or sub-Tropics where human excreta has possibly been used for fertilizer
or where these foodstuffs have been freshened with ditch water. Oysters, unless
their source is known to be safe, must not be served raw. Refrigeration at 40°
F. or lower should be provided for all food in which bacteria can multiply.
(3) Fly breeding should be energetically combatted at all times. All kitchens
and mess halls should be properly screened, with screen doors opening outward,
and all crevices closed. Fly traps, flypaper, sprays, and flyswatters should be
used in kitchens and mess halls by specially assigned personnel. All foods should
be covered whenever feasible.
(4) Sanitary disposal of excreta must be carried out strictly both in fixed
installations and in the field. (See AR 40-205.)
(5) Permanent food handlers should be examined in accordance with AR 40-205
before employment, and at regular intervals thereafter. All food handlers must be
carefully instructed and trained in personal cleanliness, especially the proper
cleansing of hands after defecation.
(6) Cases must be treated under careful enteric isolation precautions with
sterilization of excreta and bed linen, protection from flies, and personal hygiene
of attendants. Convalescents must not be discharged until stool and urine cultures
are negative. They should be recalled for periodic cultures in order to detect
possible carrier state. (See AR 40-205 and 40-210.)
(7) Sources of infection should be determined by epidemiological investigation
wherever possible, with particulai* emphasis on the discovery of carriers.
(8) Vaccination with triple typhoid vaccine must be carried out according
to AR 40-210. (See sec. VII.)
* 71.19. Paratyphoid fevers.—a. Etiologic agent.—The paratyphoid organisms
are Bact. paratyphosum A (Salmonella paratyphi), Bad. paratyphosum B (Salmonella
schottmuelleri), and other organisms of the genus Salmonella.
b. Geographical distribution.—World-wide.
c. Transmission.—Same as for typhoid fever.
d. Recognition.—Same as for typhoid fever The paratyphoid fevers are usually
milder than typhoid, with fewer complications and a shorter course. Bacteremia
frequently does not occur. There are no clinical differentiating features between
the fevers caused by different varieties of paratyphoid organisms. It must be
borne in mind that the Salmonella organisms can also cause severe bacterial food
poisoning and diarrhea, a clinical picture entirely different from paratyphoid
fever and also more prevalent in both civil and military life. (See par. 58.)
e. Specific diagnosis.—Same as for typhoid fever.
f. Treatment.—Same as for typhoid fever.
g. Prevention.—Same as for typhoid fever.
71.20. Yaws.—a. Etiologic agent.—Treponema pertenue.
b. Geographical distribution.—Common in the Tropics, especially in Africa,
Polynesia, the Philippines, and some parts of the Western Hemisphere. Prevalent
in the West Indies (especially in Jamaica, Haiti, Trinidad, Antigua, and other
islands of the Leeward group), and in coastal and valley settlements of Colombia.
c. Transmission.—By direct contact with lesions of the patient and by nonbiting
flies which convey infective material from the open lesions of the yaws patients.
d. Recognition.— (1) An initial granulomatous lesion (mother yaw) usually
appears on exposed part of body.
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(2) Generalized or secondary lesions appear in 2 to 8 weeks. These resemble
raspberries (frambesiform) or large warts, but smaller papules, or scaly, ringworm-
like lesions may appear.
(3) Later, disabling lesions consisting of hyperkeratoses with fissuring or
ulceration of the plantar epithelium may develop. Gummatous lesions like those
of syphilis may occur late in the course of the disease (gangosa—partial destruction
of the nose).
e. Specific diagnosis.—The initial and secondary lesions generally contain
Treponema pertenue, identified by darkfield examination. The blood Wassermann
and Kahn reactions usually become positive 1 or 2 weeks after appearance
of the initial lesion.
f. Treatment.— (1) Yaws responds to the same therapy commonly used for
early syphilis, but good results are usually obtained with much less treatment
than in syphilis.
(2) The preferred arsenical is mapharsen. Adult dose for males is 0.06 gram,
and for females 0.04 gram. Neoarsphenamine is also effective, 0.75 gram for adult
males and 0.6 gram for adult females. The preferred bismuth preparation is
bismuth subsalicylate in oil, dose 0.2 gram. The dose for children should be
reduced according to age and weight.
(3) The following standard course of treatment for yaws is recommended:
four weekly injections of mapharsen or neoarsphenamine and bismuth subsalicylate
given on the same day. This is to be followed without a rest period
by four weekly injections of mapharsen or neoarsphenamine alone, which in turn
is to be followed by eight weekly injections of bismuth subsalicylate alone. Take
serologic test, if possible, with eighth and sixteenth treatment.
(4) Follow the patient by clinical examinations and serologic tests at monthly
intervals for 3 months, and then at intervals of 3 months for 1 year. If a clinical
relapse occurs or if the serologic test remains positive for 6 months after treatment
has been started, repeat course of treatment outlined above.
g. Prevention.—Avoid contact with infective open lesions and take precautions
to prevent insect transmission. If troops are stationed in close proximity to
heavily infected native populations, special care should be given to prevent the
contamination of open sores and wounds by infective material. While uncommon,
cases have been reported in the white race.
71.21. Bejel.—a. Etiologic agent.—Treponema pallidum.
b. Geographical distribution.—Syria, Iraq, and Arabia.
c. Transmission.—Direct contact; possibly also by flies and other insect vectors,
and by indirect contact through unsanitary eating and drinking habits. The
exact portal and mechanism of entry has not been determined. Usually acquired
in childhood, seldom congenital; nonveuereal and rural.
d. Recognition.—Typical primary lesions such as are observed in yaws and
venereal syphilis have not been seen in bejel. Early lesions mucocutaneous;
late lesions—skin ulcers, periostitis of long bones, symmetrical depigmentation
of skin, hyperkeratoses, juxta-articular nodules, erosions of pharynx and nasal
bones; cardiovascular and nervous systems apparently not affected.
e. Specific diagnosis.—Darkfield examination of exudate from mucocutaneous
lesions in early and relapsed cases positive for T. pallidum. Blood Wassermann
and Kahn reactions become positive within a few weeks of the onset, and usually
remain so whether late lesions appear, or the disease continues latent.
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f. Treatment.—Same as for yaws.
g. Prevention.—Same as for yaws.
71.22. Yellow fever.—a. Etiologic agent.—The virus of yellow fever.
ft. Geographical distribution.—Yellow fever has previously occurred repeatedly
in severe epidemic form in most of the countries of the Western Hemisphere and
in Africa. Within recent years it has been shown to be endemic in extensive
jungle areas in tropical South America (Bolivia, Brazil, Colombia, Ecuador,
Paraguay, Peru, Venezuela, possibly in the Guianas, Eastern Panama, and elsewhere),
and in Africa. The transfer of virus from such jungle areas to rural or
urban regions where Aedes aegypti breed and the inhabitants are susceptible has
resulted in epidemics of yellow fever.
c. Transmission.—Within recent years it has been shown that there are important
differences between the transmission of endemic (jungle) and that of
epidemic (urban) yellow fever.
(1) Jungle yellow fever.—Endemic yellow fever is transmitted by other mosquitoes
as well as Aedes aegypti in tropical or subtropical forest environment.
In man there may be scattered cases or extensive epidemics. The disease is
maintained chiefly by susceptible forest animals. In Brazil Aedes scapularis,
A. fluviatilis, A. leucocelaenus, and Haemogogus capricornii have been incriminated
as effective vectors, and the last two have been found naturally infected.
Other species of Aedes and other genera native to North America, Europe, Africa,
and the Orient have also been proved to be efficient vectors in the laboratory.
(2) Urban yellow fever.—This is the aepypti-transmitted classical disease of
cities, large towns, and occasionally of rural areas. Where susceptible individuals
and Aedes aegypti are numerous the urban disease may appear in epidemic
form after the disease is introduced from areas of jungle or urban infection.
Epidemics may also result from the introduction of nonimmune troops into places
in which the endemicity of urban yellow fever is barely perceptible. Aedes aegypti
are found in the Tropics, sub-Tropics, and temporarily elsewhere, if newly introduced,
during a warm season.
d. Recognition.—Incubation period 3 to 6 days; onset sudden ; high fever with
short remission third to fourth day followed by recrudescence; pulse rate at first
rapid but begins to fall with a rising temperature; albuminuria is usually marked
on third day; black vomit; skin and mucous membrane hemorrhages; jaundice
of increasing intensity. Mortality: 10 to 30 percent.
e. Specific diagnosis.—A provisional diagnosis may be made on the basis of
symptoms. For a final decision, 30 cc of blood should be drawn early in the
disease and again 3 weeks after onset. The sterile blood specimens should be sent
to a laboratory equipped to make yellow fever protection tests. If the first fails
to protect mice against yellow fever and the second protects, the disease was
yellow fever.
f. Treatment.— (1) Specific.—None.
(2) General.— (a) Isolate the patient in a screened room.
(&) In severe cases during the acute state, give only citrus fruit juices and
alkaline water (e. g., 3,000 cc tap water with 15 grams bicarbonate of. soda
daily). In mild and moderate cases a light diet high in carbohydrates and low
in fats is recommended.
(c) Give saline laxative at onset and thereafter enemas as needed.
58
TM 8-210
GUIDES TO THERAPY FOR MEDICAL OFFICERS C 1
( * 2 fl? {JJg n fl > \
£ C '’T K 3 g o 3 1 7 ^ H 2 B S t “ s " 8. > 3 3 7 ’
5 2 S' / S “ 2 X 1 8 § ' ^ [ *
3 * K u . V - ■ i . 7 8 & 3 2 C » I
s \ & J / ~ y \ 1 ^ ’ -
2- w r \ X ^ - 3
« / p ft- ° > ^ f 4 v 2-3 B-’c
Ul. 7^ — ' ' \ ^>r~ f) p< o 3 >0 v V ^ U Z > ' d £ 2. £ V / s 2 < V S S. P- O’ 3 r? <^&3: I? »& i§ I>  3 Q - S p p P L w 9 ^»x 2- §■
3 p n g o u- 2- r- c p- 3 2 o S. £ u u * o o
*5 3 *■} 6) 6J '^L ® 2 2 n- S £ >---- p-
•“ o> r*" <■> <7 ,4- o ' > x t
-j 0 B g Sr4 g
Figu re 2.—Common carotid artery—incision, approach, and collateral
circulation.
36
TM 8-210
GUIDES TO THERAPY FOR MEDICAL OFFICERS H
(h) Avoid trauma to the bifurcation; use procaine to block the
nerve receptors in the carotid sinus.
(2) Subclavian artery—operative procedure (fig. 3).— (a) Recline
the head and turn it to the opposite side. Place sandbags
under the shoulder blades.
(&) Incise parallel to and one fingerwidth above the clavicle
over the clavicular insertion of the sternocleidomastoid muscle
to the edge of the trapezius.
(c) Section skin, platysma muscle, and branches of the supraclavicular
nerves.
(d) The external jugular vein need not be cut; better ligate
between ligatures since nicking it may produce air embolism.
(e) Section the sternocleidomastoid muscle to its sternal portion
; retract the internal jugular vein medially.
(f) Clear the loose fat from the anterior scalenus muscle;
define and retract the phrenic nerve medially.
(iz) Sever the anterior scalenus muscle with its posterior
fascia; the subclavian artery lies immediately behind it, over
the apex of the pleura; the subclavian vein lies anterior to the
scalenus muscle, between it and the clavicle; the brachial plexus
lies lateral to the artery, partially covered by the anterior
scalenus muscle.
(h) Since there is abundant collateral circulation through the
thyrocervical trunk and the internal mammary artery, ligate,
if possible, distal to these.
(3) Axillary artery—operative procedure (fig. 4).— (a) Elevate
the thorax and moderately abduct the arm.
(5) Incise the skin in the groove between the deltoid and
major pectoral muscles, beginning at the clavicle for a length
of 3 to 4 inches.
(c) Retract the edges of the two muscles and identify the
transverse fibers of the minor pectoral muscle.
(d) Identify and retract the cephalic vein.
(e) In the loose fat above the free edge of the minor pectoral
muscle, the brachial plexus, more medially the axillary artery
and medial to it the axillary vein, are visible. Since ligation
proximal to the origin of the two circumflex humeri and the
subscapular vessels is safe whereas a tie distal to these may
result in gangrene, infraclavicular ligation is preferred to that
with the customary axillary exposure, during which the dangerous
segment of the axillary artery between the subscapular
and circumflex vessels may be tied.
37
TM 8-210
11 MEDICAL DEPARTMENT
RamuS
Supra- z
SpinouS -
A.circum. _
hum. post:
A.thoracaliS
lat.
A.circuim. .
hum. ant.
RamuS deSC. . A.transverSa colli TruncuS
Ramus acomialis
RamuS
A. subscapularis
A. subscapularis
A. circumf lexa /
scapulae
A inFraScapulariS
A.intercostalis
Sup.
A.thoracaliS
sup.
TrunCus
- Costocervicalis
M. sternohyoideus
M. stemocleidomastoideuS,.'
" interna
A.interdoStaliS-
’ ramus ant.
A.inter-
,/ costal I
A. inter-
/costaLU
t r N. iudularis
J * Isiw ' d ant. Glandula
vagus' J \ thyreoidea
\ f \ A carotiscomm.
Ay tho'racicus 'A.subclavia
Figur e 3.—Subclavian artery—incision, approach, and collateral
circulation.
38
TM 8-210
GUIDES TO THERAPY FOR MEDICAL OFFICERS H
/ \i[ a ^^ieuuus^^L■th°ra-c°*
-T vk~~ (( - 'rf '((^^^’^■dromialiS
IF- l\ V Acircurnflex^gr X/ //'A.axillaris
|*p ~ ilF num.post.
F X.- C f \
V A.circur^flexa B |F A.SubScApularis
X hvim.ainr.
I «'■ f0t
A. profunda, brachii \ ||CA.bra.chialis
X
M.pectoraliS
M.deltoideuS^ . '
" ' 'M.pectoraJiS minor
Fl. ,b iceps , , . N.muSculocutaneuS [caput breve] '^^^^g^.-Nmed^nus
A. circumflexaL^^fc^^^^^'?®^" ,
humeri post. ~Axillaris
N.axillaris ' Vdl.ulnaris et n. radiahs
Fig ur e 4.—Axillary artery—incision, approach, and collateral
circulation.
39
TM 8-210
11 MEDICAL DEPARTMENT
(4) Brachial artery—operative procedure (fig. 5).— (a) Abduct
the arm in maximal supination.
(&) Incise the skin in the middle of upper arm over the bicipital
groove.
(c) Enter the fascia at the medial edge of the biceps and
retract this muscle.
(d) Isolate the thin, cutaneous antebrachii medialis nerve and
the much heavier median nerve.
(e) Retract the median nerve medially; the brachial vessels
are in its close proximity. High division into radial and
ulnar arteries may occur. No danger accompanies ligation
below the profunda brachii and superior ulnar collaterals.
(5) Cubital artery—operative procedure (fig. 6).— (a) Abduct
and supinate the arm.
(&) Bisect the lacertus fibrosus through an incision running
from the bicipital groove to the edge of the biceps tendon.
(c) Ligate and cut the median cubital vein.
(d) The median nerve is medial, lateral to it the vein, between
and behind it the artery. If the incision is too low the pronator
teres muscle is in the way. Collateral supply is abundant
unless the recurrent vessels are destroyed below the bifurcation
of the cubital artery.
(6) Iliac artery—operative procedure (fig. 7).— (a) Place the
patient flat on his back with a sandbag under the pelvis.
(&) Incise the skin from the anterior iliac spine to the pubic
tubercle, three fingerwidths above and parallel to Poupart’s
ligament.
(c) Tie and cut the superficial epigastric vessels and sever in
the same direction the aponeurosis of the external oblique,
cutting across the internal oblique and transversalis muscles
and the transversalis fascia; do not open the peritoneum.
(d) With the two index fingers bluntly dissect off the peritoneum
from the psoas muscle and retract it together with the
ureter, medially and cephalad; on the right the vena cava
divides just behind the common iliac artery; the right common
iliac vein first lies lateral to the artery, then passes behind it
to its medial side; the left common iliac vein lies altogether
medial to the artery.
(e) Collateral circulation following ligation of common iliac
artery goes through the internal mammary, superior and inferior
epigastrics, superior hemorrhoidal, lumbar, and middle
sacral arteries; it is insufficient in sudden occlusions but satis-
40
TIM 8—210
GUIDES TO THERAPY FOR MEDICAL OFFICERS H
A. collatoralls
uln inf.
A.recun__
radialis /
'~rrT77ff7'
A.rad.
A. profunda
brachii
A.profi
brachii -
ant.
approach, and collateral
A. brachialis
A.collaterals
ulnaris sup.
Figur e 5.—Brachial artery—incision,
circulation.
-A. etV.
\ brachialis
v Fl. triceps brachii
\ [caput lonp.J
A.'Col lateralis
uln. sup.
N. triceps brachii
[caput med]
M. bicep:
brachii
N. ulnaris
A.recurrens
ulnaris ant.
'A.recurrens
ulnaris post.
A. ulnaris
N. musculocutaneus
brachialis
N. medianus
-N.cutaneuS antibrachii
med.
V basilica
41
TM 8-210
11 MEDICAL DEPARTMENT
A.collateralis _
ulnaris Sup.
A. profunda brachii
A.brachialiS --
A.recurrenS
radlalis
Tendo m. bicipitis
brachii ' ’L aceI rtus fibrosis
N-Cutaneus ' I A.collateralis
anti brachii lat. ulnaris inf.
V.cephaliCa,J ' ' ! A.brachialis
A.collateralis _
ulnaris inf.
A.profunda
brachii ant. >
M.brachioradial
iS
t A. recurrens
\ ulnaris ant.
A.recurrent
ulnaris po$t.
'A.ulnari$
/ M.pronator \ 'A.mterossea
, teres 'v communis
V.bracHialis , Kmedianus X.radialis
M. brachial ip
Fig ur e 6.—Cubital artery—incision, approach, and collateral
circulation.
42
TM 8-210
GUIDES TO THERAPY FOR MEDICAL OFFICERS H
A. ci rcumf lexa
ilium prof.
Asjlutaea Sup.
A. iliolumbalis
A. epigastrica inf.
\ A. iliaca comm.
•A.obtur-
A. glut,
inf.
\ A. pudenda mt
A.circum. fem.med.
A. hypoi.
iliada " gastrica.
ext. ~ ~'
A. Ci rcumflexa
fem. lat.
A.profunda fem.
A. femoral!^
Fig ur e 7.—Iliac artery—incision, approach, and collateral circulation.
M. obliq. ext. abd.
,. _ M.obliq-. int. abd.
JI,-Fl. trang. abd.
- - Peritonaeum
"Ureter
''-Aa.iliaca comm.
'•V cava inf
Vertebra lumb.V
'‘•FI. psoas major
43
TM 8-210
H MEDICAL DEPARTMENT
factory in slowly developing ones or in aneurysms. Collateral
circulation after ligation of the external iliac artery is much
better. The two important vessels are the circumflex iliac
profunda and the deep epigastric as through them the hypogastric
artery can feed the femoral, hence the external iliac
artery should be tied above the origin of these two vessels.
(7) Femoral artery—operative procedure (fig. 8).— (a) Place
the patient flat on his back with a sandbag or kidney rest to
hyperextend the thigh.
(b) Incise the skin from the middle of Poupart’s ligament in a
longitudinal direction for 4 inches (or alternatively, parallel
to and two fingerwidths below Poupart’s ligament).
(c) Identify Poupart’s ligament and clear the fascia lata of
fat and the lymph nodes just below it.
(d) Incise the fascia lata longitudinally; the femoral vein is
most medial, next lies the artery, and most lateral the nerve;
the major saphenous vein leads to the femoral artery.
(e) Collateral circulation is established through the inferior
gluteal and medial circumflex to the popliteal artery; ligation
below the profunda opens another important channel to the
popliteal artery through a perforating branch. Tie, if possible,
below the profunda.
(8) Popliteal artery—operative procedure (fig. 9).— (a) Place
the patient on his abdomen with a sandbag under the knee.
(b) Make a generous longitudinal incision through the middle
of the popliteal space, incising the fascia; tie or retract the
small saphenous vein.
(c) In the loose fat, closer to the lateral wall of the space
(biceps), the tibial nerve is encountered, isolated with a nerve
tape and laterally retracted; below and medial is the vein,
deepest and most medial the artery.
(d) The collateral supply is poor at this level; the channels
operating on closure of the femoral enter the popliteal artery
above the fossa where there are no large masses of muscle and,
hence, small collaterals. If ligation is unavoidable, the tie
should be placed above the interior collaterals.
(e) Simultaneous vein ligation and sympathetic block are important.
Arterial suture is preferable to ligation; this caution
is unnecessary in aneurysms of more than 6 weeks’ duration.
(9) Anterior tibial artery—operative procedure (fig. 10).—
(a) Place the knee in full extension with the patient on his back.
44
TM 8-210
GUIDES TO THERAPY FOR MEDICAL OFFICERS H
A. prof,
fem.
A.iliaca ext
A. femoraliS
A.circum.
fem. lat.
A. cirdum.
fem. lat. \
A.circam.
fem. med?
A.‘glut. inf.
A. pro. fem.
[rami pert]
A. femoralis
N. femoralis
Msartonus /
V saphena magna
'V. femoralis
M. iliopsoas x Pectineu5
A. profunda femoris
Figur e 8. —Femoral artery—incision, approach, and collateral
circulation.
45
TM 8-210
11 MEDICAL DEPARTMENT
A.^enu Sup.
medialiS '
A. poplitea—
Tendo m. Semitendinosi
M.sartorius i M.SemimembranosuS
V saph.
parva
A poplitea , M.biceps femoris
v. poplitea
A.genu mf._
medialiS
N. tibialis
A.fienuin£
'lateralis
A.eenu Sup.
lateralis
A A.recur.
/ 'tibialis
/ ant.
x A. tibialis
' ant.
A. tibialis
post.
Fig ur e 9. -—Popliteal artery—incision, approach, and collateral
circulation.
46
TM 8-210
GUIDES TO THERAPY FOR MEDICAL OFFICERS H
A.malleolaris
ant.
A. peronaea-
A. genu ’inf.
lateralis"
A.recurrenS
tibialis ant.
A.$5enu sup.
lateralis
N.' peronaeus
M. tibialis
ant.
.A.genu.
inf. med.
A. tibialis
’ post.
A. malleo-
- Laris ant.
\ med.
--rl. tibialis
post.
'A.et V.
tibialis ant.
A. tibialis
ant.
Mm. extensores
lon£i di$5itorurn
et halluciS
Figu re 10. —Anterior tibial artery—incision, approach, and collateral
circulation.
47
TM 8-210
11 MEDICAL DEPARTMENT
(&) Incise the skin in the middle of the lower leg, a thumbwidth
lateral to the lateral margin of the tibia, for a distance
of 3 to 4 inches.
(c) Split the muscle fascia and carefully identify muscle space
between the anterior tibial and the long extensor digitorum
muscles.
(d) Retract these apart and expose, within the cylinder of
fat, the vein, artery, and nerve, which approach the tibia from
above downward. There is abundant collateral circulation from
the posterior tibial and peroneal arteries. Ligation of both
anterior and posterior tibial arteries is only safe if the peroneal
is intact.
(10) Posterior tibial artery—operative procedure (fig. 11).—
(a) With the patient on his back, rotate the thigh externally and
place a sandbag under the bent knee.
(b) Incise the skin for a length of about 3 inches in the middle
of the lower leg, % inch medial from the internal margin of
the tibia.
(c) Isolate and retract the saphenous vein and nerve in the
subcutaneous fat.
(d) Sever the insertion of the soleus muscle from the tibial
shaft and retract the belly of this muscle.
(e) Cut the deep fascia longitudinally; toward the tibia, the
fibers of the flexor digitorum longus and the posterior tibial
muscle become visible; the neurovascular bundle lies against
the latter muscle. The tibial nerve should be carefully isolated
; the peroneal vessels are found deeper in the wound. The
main collateral of the posterior tibial artery is outside of the
anterior tibial artery, the peroneal branch. When both posterior
tibial and peroneal arteries are injured, ischemia of the
limb may become quite pronounced.
g. Repair of the artery should only be attempted when special
suture material and assistance are available, and when the
procedure holds promise of producing a useful limb.
h. A pulsating hematoma should not be subjected to emergency
treatment, but should be left for deliberate treatment,
later.
i. Arterial spasm may be associated with injury to, and
especially thrombosis of, the companion vein. It may be due
to a blow or a nearby flesh wound, and should be suspected
48
TM 8-210
GUIDES TO THERAPY FOR MEDICAL OFFICERS H
A. redur. tib. ant.
A. tibialis post
Tibia —
Fibula --
A.peronaea --
A.peronaea ant.
V Saph.ma
M, flex-dip.
lonp.
M. tib. post
Ramu$ comm.
N. SaphenuS A.peronaeapo$t
V. et. a. tib.' J
post.
A. et. v. peronaea
N .Tibialis ' t
IT. Soleu?
A.malleolaris
post. lat.
A.rnalleolariS
P°3t.rned.
A.dal. lat-J
A. dal. med.;'
CaldaneuS
Fig ur e 11.—Posterior tibial artery—incision, approach, and collateral
circulation.
49
TM 8-210
11-12 MEDICAL DEPARTMENT
when the limb is pulseless and cold in the absence of direct
evidence of hemorrhage. It should be treated by the application
of warmth to the body, the intravenous injection of 0.03
gram (% grain) papaverine, sympathetic block, or a combination
of these measures.
j. Arteriovenous fistula is unlikely to be detected in conditions
of emergency, but bruit, thrill, or local arterial pulsation may
rarely appear early; it does not call for emergency treatment.
12. Sprains, strains, and contusions.—a. General.— (1) The
use of the words “sprain” and “strain” is very much confused,
but a sprain is usually considered to involve ligamentous
tissue, and a strain, muscle or tendon tissue; the term “contusion”
means a bruise, with consequent rupture of the capillaries
in the involved tissues.
(2) All surgical treatment is aimed at shortening to a minimum
the convalescent period—of course within the limits of
safety—but this phase of treatment is apt to be overlooked in
sprains, strains, and contusions.
(3) In acute sprains, strains, and contusions, the treatment
should include (within the first hour, if possible) cold and
compression to minimize the hemorrhage and the hematoma, and
to shorten the period of hematoma absorption and healing;
such treatment not only reduces the period of absorption but
also decreases to a minimum the amount of fibrous scar laid
down in the tissues.
(4) A ligament, muscle, or tendon is more often partially
rather than completely torn across; only complete tears require
operative surgical interference, and all those, particularly in
sprains, do not require operation if the treatment is thorough.
b. Treatment.— (1) Make an accurate diagnosis of the ligaments,
tendons, and muscles involved.
(2) Immediately apply a compression bandage by placing a
properly cut piece of sponge rubber (% inch thick) or a loose
roll of cotton wadding over the region of the injured tissues
and holding it in place with an elastic bandage, the whole area
being kept cool with ice, if possible; never use strapping of
adhesive tape.
(3) Rest the injured part for 24 to 48 hours; never permit
immediate weight bearing in a sprain or strain involving the
lower extremities.
50
TM 8-210
GUIDES TO THERAPY FOR MEDICAL OFFICERS 12-13
(4) During the convalescent treatment, promote recovery and
the stimulation of lymphatic absorption of the waste products
of the hematoma by the application of heat and by massage, still
using the compression bandage as a support between treatments;
graduated physical activities may be permitted as healing takes
place.
(5) In ligament sprains when tenderness has completely
subsided and function has been completely restored, the injured
part may be considered healed; then permit participation in
active exercise, but only with adequate protection—by adhesive
tape support if exercise involves or may involve a strain on
the injured tissues.
(6) If a considerable amount of scar tissue is formed in an
area of injured tendon or muscle tissue, it will always be a
weak point, liable to recurrent injury; when undue strain is
expected, protect the previously injured muscles and tendons
by a supportive elastic bandage.
13. Fractures.—a. General.— (1) Death following fractures
occurs early as a result of shock or hemorrhage or late as a
result of infection. The dangers of all three are increased by
transportation without proper traction splints; hence, the
dictum: Splint where they lie.
(2) Immediately following a fracture, especially one produced
by gunshot wounds, there is a period of paralysis of the muscles
of the extremity, which is soon followed by one of spasm, when
the muscles contract, thus driving the bony fragments into the
soft tissues and thereby causing pain and shock; with early
splinting, before the period of spasm has begun, this is avoided.
t>. Treatment.— (1) The relief of pain, the treatment of shock,
and the administration of chemotherapeutic and prophylactic
agents should follow the recommendations given elsewhere
(pars. 14, 15, and 51).
(2) If the fracture is compound, the clothing is cut away
from the wound, hemorrhage is controlled (par. 11), and an
occlusive dressing, a first-aid-packet dressing or a shell-wound
dressing, depending on the size of the wound, is applied; make
no attempt to cleanse or debride the wound.
(3) The extremity is splinted as follows:
(a) For fractures of the femur, fractures about the knee
joint, or of either or both bones of the leg above the ankle, a
hinged half-ring splint is used.
51
TM 8-210
13-14 MEDICAL DEPARTMENT
(b) For fractures of the upper extremities, including those
about the shoulder and elbow, the Murray-Jones traction splint
is used.
(c) For fractures of the wrist and hand, a padded-board
coaptation splint is used.
(d) For fractures of the ankle and foot, a wire-ladder splint
is used.
(e) For* fractures of the spine, moderate extension is indicated
; this can be accomplished with the patient prone or recumbent,
but in the latter position a rolled blanket of pillows must
be placed under the site of injury (par. 4).
(f) For fractures of the neck, improvised support, with moderate
extension, is provided.
(<7) For fractures of the pelvis, a swathe about the pelvis,
with the thighs and legs fixed together by bandages, is applied.
(h) Detailed information in regard to the construction and
application of the splints is contained in FM 8-50.
(4) A fracture or wound in which a joint is involved should
be treated like a compound fracture, no attempt being made to
cleanse the wound.
(5) The patient is immediately transported to a hospital,
care being taken that he is properly covered with blankets, to
maintain body heat.
14. Relief of pain.—a. General.— (1) Relief of pain following
injury is of the utmost importance, not only because it
alleviates suffering but also because pain is one of the main
contributory factors in surgical shock.
(2) Pain may be relieved in two ways, neither of which
should be omitted without cause:
(a) First, proper first-aid treatment should be given, if possible,
to the injured part; thus, the application of a traction
splint to a fractured extremity, of a tight swathe to certain
types of chest injury or of a firm supporting bandage to a flesh
wound frequently results in complete or partial relief of pain.
(b) Secondly, sedatives of the proper sort and in proper
amounts should be given whenever indicated, particularly before
painful first-aid manipulations or before transportation.
(3) Sedation is accompanied by depression of the heat-regulatory
mechanism, hence extra precautions should be taken to
protect the sedated patient against the effects of cold.
52
TM 8-210
GUIDES TO THERAPY FOR MEDICAL OFFICERS 14-15
ft. Methods of sedation.— (1) For severe injuries and severe
pain, morphine is the drug of choice and should, if possible, be
given hypodermically.
(a) Inject 0.016 gram (% grain) morphine sulfate and repeat
according to the amount and duration of the relief experienced.
(&) Pain is an antidote for morphine, and a rugged man with
an excruciatingly painful injury may require three injections
at 15-minute or 30-minute intervals before relief is experienced;
however, if the respiratory rate is below 14 per minute, the
dose should not be repeated.
(c) Morphine should never be given to unconscious patients or
those with a head injury or with actual or potential respiratory
embarrassment.
(2) The barbiturates are particularly useful for moderate
degrees of pain associated with fear, emotional distress, or
nervousness.
(a) Give 0.15 to 0.30 gram (2% to 5 grains) barbital or
phenobarbital by mouth, previously dissolving the drug in a
warm fluid, if possible; or, inject 0.15 to 0.30 gram (2% to 5
grains) barbital sodium or phenobarbital sodium intramuscularly.
(b) The dose may be repeated in 3 hours, if necessary.
(c) Often the combined use of morphine and a barbiturate is
more effective than either one alone; however, full doses should
not be repeated as often as when given alone.
(3) For minor degrees of pain, acetylsalicylic acid (aspirin)
in 0.6-gram (10-grain) doses every 2 hours, is recommended.
15. Secondary or wound shock.—a. Mechanism.— (1) Primary
shock refers to a condition of collapse that may follow
quickly after the receipt of an injury; it is usually to be explained
on a neurogenic (reflex or psychic) basis. Measures
that may be of aid in treatment include the recumbent position,
the giving of stimulants, the application of heat, the relief of
pain, and the use of vasoconstrictor drugs. An early favorable
response is usually obtained, unless it is complicated by blood
loss or other shock-producing factors. This type of shock is
usually of short duration, although it may progress into the
secondary type.
(2) (a) Secondary or wound shock is usually slower in
onset than primary shock and is most apt to develop an hour
or longer following injury. The predominant feature is a
53
TM 8-210
15 MEDICAL DEPARTMENT
marked decrease in circulation, generally produced by the loss
of an effective blood volume, which, in war, usually results
from hemorrhage. The output of the heart declines before the
blood pressure, and hence a marked decline in the blood pressure
is more than a danger signal; it indicates a marked
impairment of the blood supply to the tissues, with resulting
anoxia, which, in turn, produces a general increase of capillary
permeability, with loss of plasma from the vessels.
(b) The reduction of the blood volume in secondary shock
may be due to a loss of whole blood or blood plasma or both.
Dehydration, fatigue, pain, fear, exposure to cold, and other
factors may contribute to its origin. During the early stages
of the development of shock due to the loss of whole blood,
dilution of the red blood corpuscles usually results, unless the
subject is markedly dehydrated. During the terminal stages
of prolonged shock from any cause, even hemorrhage, a genera]
increase in capillary permeability with plasma loss and hemoconcentration
may result. Hemoconcentration is observed
throughout the early stages of shock, and largely results from
a generalized plasma loss into the tissues. A diminution in
the blood volume caused by plasma loss is more dangerous than
the same reduction due to hemorrhage. The combination of
the loss of whole blood and plasma may be such that there is
no alteration in the concentration of the red blood corpuscles.
(c) There is no infallible, easily performed laboratory procedure
which acquaints one with the condition of the circulation
in the incipient stage of shock.
b. Clinical picture.— (1) There is no difficulty in the recognition
of the advanced stages of shock. The findings include
pallor, weakness, cold extremities, rapid pulse rate, low blood
pressure, sweating, and frequently, vomiting. Unfortunately,
treatment is often of no avail when the advanced stages have
been reached.
(2) The clinical recognition of the early stages is not so
easy. Pallor and tachycardia, which are the usual findings in
early shock, may be caused by other disturbances. A history
of injury in a patient with cold, pale skin and a pulse rate
greater than 100, particularly if these abnormalities persist for
a number of minutes, usually means incipient shock. Treatment
should be instituted immediately, even though the systolic
blood pressure is not below 100. It should be remembered that
54
TM 8-210
GUIDES TO THERAPY FOR MEDICAL OFFICERS 15
the arterial pressure is being maintained by vasoconstriction
and is likely to decline rapidly with the slightest development
of shock. The reduced blood volume, vasoconstriction, and
lowered blood pressure cause diminution in tissue circulation,
and if this state is continued too long, the oxygen lack causes
irreparable damage. Signs of progression of shock include a
further increase in pulse rate, a decrease in the pulse pressure,
an increase in pallor, and sweating.
c. Treatment.— (1) General.—The prevention of fully developed
failure of the peripheral circulation is the most important
phase of treatment. The patient in profound shock
may be unable to recover even if his blood volume is fully
restored with blood itself. The clinician should recognize the
early signs and should immediately carry out the therapy that
is indicated. It cannot be emphasized too strongly that success
usually depends on the promptness with which the proper treatment
is instituted. It is generally agreed that the best single
form of therapy consists in augmenting the reduced blood
volume by the introduction of blood or blood substitutes. An
estimate should be made of the factors that are contributing
to the shock, such as dehydration, continued bleeding, cold,
pain, and fear, and various corrective measures should be performed.
The treatment that can be given by various medical
units is dependent on the facilities that are available and on
military operations or enemy action at the time; however, one
should always approach the ideal as nearly as possible.
(2) Arrest of hemorrhage.— (a) This is by far the most
important step. The available means for arresting hemorrhage
in the very advanced positions in active engagements are usually
limited to digital pressure on the artery between the w’Ound
and the heart, the application of a tight dressing, the insertion
of a sterile gauze pack, and the use of a tourniquet (par. 11).
A tourniquet should usually be employed only when other
means for controlling hemorrhage are inadequate. There is
no objection to placing a tourniquet on an extremity that is
injured beyond repair. With civilian casualties, where it is
known that the constriction can soon be released, the tourniquet
should find a more extensive field of usefulness than in field
operations. A fractured limb should be splinted during transport.
This lessens the additional loss of blood and plasma at
the site of injury and reduces the severity of the pain.
55
TM 8-210
15 MEDICAL DEPARTMENT
(&) When the casualty has been transported to a place where
adequate facilities are available, it should be noted whether or
not the bleeding has stopped. If it continues, isolation of the
blood vessel and its ligation and division may be necessary
(par. 11). If a tourniquet is in place and an amputation is
to be performed, the tourniquet should not be removed until
the time of or after the amputation. Preliminary removal of
the tourniquet is followed by the passage of a considerable
part of the blood volume into the dilated peripheral blood
vessels and by the further loss of whole blood and plasma
from the injured vessels. If the tourniquet is removed and
an attempt to save the part is to be made, facilities for blood
transfusion should be available.
(3) Relief of pain.—There is convincing evidence that morphine
in doses of 0.016 to 0.032 gram (^4 to % grain) is of aid
in the prevention of shock. Larger amounts or doses at too
frequent intervals may result in depression of the respiratory
center. It should be given for the pain and restlessness associated
with injuries, except all intracranial ones, before the
patient is moved from the scene, and is preferably injected
subcutaneously or intramuscularly, although it may be given by
mouth. Sodium phenobarbital in doses of from 0.18 to 0.30
gram (3 to 5 grains) parenterally should be given for the
restlessness associated with intracranial injuries.
(4) Body temperature.— (a) Every effort should be made to
prevent and to correct excessive chilling. Stretcher bearers
should be familiar with the correct use of waterproof sheets
and blankets. When blankets are not available, protective
clothing should be placed between the canvas of the stretcher
and the patient. More protection is needed under the body
than over it. Wet clothing should be removed and dry garments
should be substituted as early as possible.
(b) When facilities are available, the chilled patient should
be warmed by artificial means. This may be accomplished by
hot-water bottles, by warm bricks or stones wrapped in blankets,
or by more elaborate means, such as a heat cradle or an electric
blanket. Unless contraindications exist, warm fluids may be
given by mouth or by rectum.
(c) It should be realized that excessive heat may cause as
severe ill effects as excessive cold. Peripheral vasodilation due
to overheating may cause a decrease of the blood flow to the
more vital structures.
56
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GUIDES TO THERAPY FOR MEDICAL OFFICERS 15
(5) Restoration of blood volume.—It is generally agreed that
the intravenous introduction of whole blood and blood substitutes
is the most valuable single method for preventing and
combating shock. It has been emphasized that the blood volume
should be restored before general capillary damage takes place.
The quantity of blood that is given should be governed by the
needs of the patient. If one pint is not effective in restoring
an effective blood volume, it does not follow necessarily that
three or four pints will not result in permanent benefit.
(a) Whole blood is of value in the treatment of shock,
regardless of whether the decrease in the blood volume is due
to hemorrhage or to the loss of plasma. There are many features
about the use of whole blood that frequently makes its
employment impracticable under field conditions. These include
difficulties in preservation, in transportation, and in making
compatibility tests. There is, however, no valid objection
to the use of fresh or preserved (for not more than 8 days)
blood, if these obstacles can be overcome.
(6) Liquid blood plasma and serum present advantages over
whole blood: compatibility tests are not necessary and the
keeping qualities are superior. Most cases of shock are associated
with hemoconcentration; hence a given quantity of plasma
or serum is more effective in treatment than an equal quantity
of whole blood. Furthermore, blood plasma and serum are
approximately as effective in the treatment of hemorrhage as is
whole blood. One objection to the use of these fluids in advanced
stations is the fact that ideally they should be stored
at icebox temperature.
(c) Dried blood plasma and serum (fig. 12) present the
advantage, if properly prepared, of prolonged preservability.
Denaturation is slow, and the multiplication of bacteria is retarded.
Exposure to moisture must be avoided. Compatibility
tests are not necessary. One has only to dissolve the powder in
distilled water and to introduce the solution intravenously.
(d) Isotonic salt and glucose solutions are useful in the
treatment of shock when plasma or serum are not available.
Restoration of the blood volume, however, is only temporary,
since the fluid rapidly leaves the blood stream. Furthermore,
the intravenous introduction of large quantities of solutions of
crystalloids in the presence of capillary damage may result in
the loss of a large amount of protein from the blood vessels.
57
TM 8-210
15 MEDICAL DEPARTMENT
DIAGRAM 'A
RESTORa TiSN OF
the dr ied pla sma
COTTON
FILTER
RESTORED I
PLASMA I
iw /plc*WAY r/
SHORT //
needle « K_>/
fflfl-CLAMD
J plasm a
FILTER
L OBSERVATION
4 Tue,t-
D INTRAVENOUS
J*- NEEDLE
| DIAGRAM 'B~
Figu re 12.—Standard Army and Navy package of dried human plasma.
Instructions for use.—1. Open metal cans with attached keys.
2. Remove plasma and water bottles. Cleanse stoppers with alcohol.
3. Remove cellophane from double-ended needle and remove glass tube
from one end of needle.
4. With water bottle in upright position insert uncovered end of
double-ended needle through stopper into the water bottle.
5. Remove cellophane and glass tube covering airway needle and in-
58
TM 8-210
GUIDES TO THERAPY FOR MEDICAL OFFICERS 15
sert needle of airway assembly through rubber stopper into the water
bottle.
6. Elevate free end of airway assembly to prevent water from wetting
cotton filter in airway. Caution: If cotton in airway filter becomes wet—
remove it.
7. Remove glass tube from other end of double-ended needle, invert
water bottle and insert needle through stopper into plasma bottle.
(See diagram A.)
8. Allow water to be drawn in plasma bottle.
9. After water is added, double-ended needle is removed from plasma
bottle.
10. Shake plasma bottle until plasma is completely dissolved.
11. Apply metal clamp to the 2" piece of rubber tubing on the intravenous
set and close it.
12. Remove coverings from short needle attached to intravenous set
and insert through stopper of plasma bottle.
13. Withdraw needle of airway assembly from water bottle and insert
through stopper into plasma bottle.
14. Invert plasma bottle and suspend it for administration. (See
diagram B.)
15. Fix glass end of the airway assembly with the suspension tape
above the inverted plasma bottle.
16. Remove cellophane from Observation tube and intravenous needle.
17. Attach intravenous needle to tube and remove glass tube from
needle.
18. Loosen metal clamp and allow plasma to fill rubber tubing. When
tube is filled, tighten metal clamp.
19. Insert needle in vein and regulate flow with screw clamp. If
patient is to receive additional plasma, restore second bottle as outlined.
Close regulating clamp as soon as first bottle is empty, but before air
enters tube. Pull out needles from first bottle and insert in second
bottle. Elevate end of airway and fix it in place with the suspension
tape. Caution: If vacuum in plasma bottle is lost, apply pressure in
water bottle by forcing air into airway tube. If this method fails, remove
stoppers and pour water into plasma bottle. Replace stopper on
plasma bottle and administer immediately.
It is in the correction of conditions that may lead to shock,
such as dehydration, that these solutions find their greatest
usefulness.
(e) Hypertonic solutions of crystalloids are rarely indicated
in the prevention and treatment of shock.
(f) Gum acacia in saline solution may be effective, but it is
much more dangerous than plasma or serum and probably should
not be used.
(6) Correction of dehydration.—Dehydration is one of the
most frequently encountered contributing agents in the devel-
59
TM 8-210
15 MEDICAL DEPARTMENT
opment of shock. Since the loss of water is accompanied by the
loss of salts, fluids that are given by mouth or otherwise should
contain salt (drinks should contain half a teaspoonful of salt to
the pint). Unfortunately, many injured patients are unable to
retain fluids when given by mouth, and other routes are therefore
frequently necessary. If the condition of the circulation
is such that fluid can be absorbed from the subcutaneous tissues
or rectum, these routes are preferable to intravenous injection.
If intravenous therapy is necessary, it is well to alternate the
giving of isotonic saline solution with that of whole blood or
plasma. As stated previously, the intravenous injection of
large quantities of solutions of crystalloids may result in damage.
Excess salt solution may cause edema, and 5 percent
glucose solution should be alternated with or mixed with saline,
particularly if edema is present.
(7) Oxygen inhalations.—Tissue anoxia occurs in shock and
is somewhat relieved by the inhalation of a high concentration
of oxygen (95 percent or higher). As a matter of fact, the
benefit is not striking, the apparatus is cumbersome, and
usually one’s efforts had better be expended in some other form
of therapy.
(8) Vasoconstrictor drugs.—Vasoconstriction is usually present
in secondary shock except in the terminal stages, and the
production of additional vasoconstriction may result in harm
rather than benefit. An increase in the blood volume and in the
effective flow of blood to the tissues, rather than solely an
increase in the blood pressure, are to be desired, and these
changes can be accomplished most satisfactorily by the introduction
of blood or blood substitutes. In primary or neurogenic
shock, vasoconstrictor drugs may be given, as previously
indicated.
(9) Adrenocortical extract.—Potent extracts have been available
only a short while, and evidence as to their effectiveness
is somewhat controversial.
(10) Anesthesia.— (a) Whenever possible, local anesthesia
should be used for patients in shock. If an inhalation agent is
used, it should be combined with an adequate quantity of
oxygen, since anoxia is already present. For this reason, oxygen
and ether is preferable to oxygen and nitrous oxide, since
the latter mixture generally results in cyanosis.
(6) General anesthesia should be avoided or postponed,
60
TM 8-210
GUIDES TO THERAPY FOR MEDICAL OFFICERS 15-16
whenever possible, until the shock has been treated and the
patient’s condition has improved. Disastrous consequences frequently
result from a failure to appreciate the danger of general
anesthesia in a critically wounded patient.
16. Respiratory emergencies.—a. General.—A respiratory
emergency is any marked interference with the transport of
oxygen to or carbon dioxide from the central nervous system.
b. Mechanism.—It may result from one or more of the following
:
(1) Decrease of respiratory exchange.
(2) Obstruction of the upper respiratory passages due to
tongue position, edema, or spasm from irritants.
(3) Blocked alveolar absorbing surface caused by blood,
water, vomitus, fibrosis, or pneumonitis.
(4) Marked decrease in the rate of flow or quantity of circulating
blood.
(5) Interference with the normal negative pressure of the
pleural cavity (wounds of the chest wall and diaphragm—
pneumothorax).
c. Causes.—The etiologic agents are shock, hemorrhage of
the upper respiratory tract, drug overdose, gas poisoning, immersion,
vomitus, edema, blood or pus collections pressing on the
respiratory tract or rupturing into it, brain injury, paralysis,
and wounds of the thoracic wall, viscera, face, or neck.
d. Signs and symptoms.—These are as follows:
(1) Inadequate, labored, noisy, rapid, or dyspneic breathing,
or apnea.
(2) Pulse abnormalities.
(3) Pale, ashen-gray, or cyanotic color of the skin.
(4) Mental disturbances (overconfidence, delirium, or unconsciousness).
(5) Muscular disturbances (tremors or convulsions).
e. Treatment.—Attempt to relieve respiratory obstruction and
to restore the proper oxygen and carbon dioxide transport as
follows:
(1) The patient should be placed laterally with the head
down, or prone if fluids or foreign bodies are suspected. The
mandible and head should be adjusted so that they are in proper
relation to the cranium and thorax, respectively; pull the tongue
forward.
(2) If a foreign body is present in the pharynx, larynx, or
439700°—42----- 3 61
TM 8-210
16-17 MEDICAL DEPARTMENT
trachea, an attempt should be made to remove it. Try a sharp
blow on the back, with the body suspended head down, or
wiping, or suction, if available. Endotracheal suction with
direct vision through a laryngoscope may be tried, if necessary,
and if the apparatus is at hand.
(3) It may be necessary to establish an artificial airway. A
rubber tube passed down to the larynx or into the trachea
through the mouth or nose, either blindly or with an anesthetist’s
laryngoscope, is often life-saving. In the presence of hemorrhage,
a pack should be placed firmly around such a tube. Remember
that a tracheotomy can be performed with a pocketknife.
(4) In cases due to the inhalation of an irritant gas, with
acute laryngospasm and edema, the following emergency treatment
should be given:
(a) Spray into the upper respiratory tract during attempts at
inspiration a 5 percent cocaine solution, nebulized to as fine a
cloud as possible.
Caution: It should be remembered that cocaine is extremely
toxic to some individuals. A solution of this strength should be
used only as an emergency measure, and then only in such
amounts as the emergency warrants.
(&) Administer the richest oxygen atmosphere obtainable.
(5) If inadequate ventilation is due to drug depression, head
injury, open pneumothorax, shock, hemorrhage, or partial obstruction
that cannot be removed, oxygen enrichment of the inspired
air is beneficial. Always use it if available.
(6) (a) If exchange is inadequate and oxygen is not available,
respiration may be enhanced by—
1. Mouth-to-mouth, mouth-to-nose, or mouth-to-artificialairway
breathing.
2. The Schaefer maneuver (see par. 29).
(6) If respiration is absent, attempt to reestablish it by these
methods instantly; the airway must be patent (see above).
17. Burns.—a. General.—Burns, as discussed in this paragraph,
include all cases with damage of the skin and underlying
tissues due to heat, chemicals, or electricity.
b. Fundamentals of treatment.— (1) The prevention and control
of shock is the primary consideration in the management
of every burn.
(2) Proper prophylactic measures against pyogenic infection,
tetanus, and gas gangrene should be taken.
62
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GUIDES TO THERAPY FOR MEDICAL OFFICERS 17
(3) Satisfactory encl results, that is, minimal scar formation,
largely depend on the avoidance of pyogenic infection; the moist
surfaces of burns provide ideal conditions for bacterial growth,
and it is therefore of paramount importance to employ, if possible,
strict aseptic technic in operating on and dressing burns.
c. Treatment.—(1) Proper steps for the prevention or treatment
of shock (par. 15) should be instituted.
(2) In all cases with moderate to severe burns, prophylactic
chemotherapy should be administered. Sulfadiazine is the drug
of choice (sulfanilamide may be substituted), with an initial
dose of 2.0 grams (30 grains) and subsequent doses of 0.5
gram (7% grains) every 4 hours, the small doses being necessitated
by the possibility of impaired kidney function. If normal
kidney function can be clearly demonstrated, larger doses of
sulfadiazine can be given (1.0 gram every 4 hours).
(3> Prophylaxis against tetanus (par. 49) is indicated in all
patients with second or third degree burns.
(4) A prophylactic dose of gas-bacillus antitoxin (par. 48)
may be given at the discretion of the medical officer.
(5) The burned area should be treated as follows, standard
operating room technic, if possible, being employed; with the
patient, as well as all attendants, fully masked:
(a) The burned area and then, separately, the surrounding
skin are carefully cleansed with neutral soap and water; ether
or benzene is used to remove grease, if present.
(b) All blisters and loose shreds of epidermis are carefully
removed, and this material is saved for bacteriologic study, if
feasible. Skin that gives evidence of irreparable damage
through its full thickness should be excised (evidence of irreparable
damage to deeper layers of skin may not be apparent for
several days, and excision in such cases should be done as a
secondary procedure). The resulting wound should be handled
like any other open surgical wound, primary grafting of skin
being carried out, if conditions permit. For painful surgical
procedures or dressings, general anesthesia, preferably obtained
by intravenous injection, should be employed.
(c) Burns of all surfaces except the hands, face, and genitalia
are to be treated with tannic acid and silver nitrate. A freshly
prepared 10 percent aqueous solution of tannic acid is sprayed
over the burned area. This is followed immediately by spraying
the area with a mixture of equal parts of 10 percent tannic acid
and 10 percent silver nitrate solutions. This mixture should
63
TM 8-210
17 MEDICAL DEPARTMENT
then be sprayed on the burn every half hour for a total of four
applications. If a satisfactory eschar has not been formed,
spraying of the mixture should be continued until the objective
is attained. Care should be taken to avoid normal skin about
the wound. While drying, the burned area may be kept exposed
to the air in a heated cradle. After the eschar is dry, it may be
covered by a dry sterile dressing.
(d) In the absence of infection, the eschar should be allowed
to separate spontaneously. If infection develops, the eschar
must be removed from the entire infected area, and the latter
should then be treated like any other infected wound, with the
employment of appropriate systemic and local therapy (par.
51).
(e) Tanning has been found to be undesirable in burns of the
hands, face, and genitalia. After thorough surgical cleansing,
burns of these areas should be covered with a generous application
of an aqueous emulsion containing 5 percent Of sulfadiazine.
If this is not available, boric acid ointment may be substituted.
The burned area should then be covered with a fine mesh gauze
(44-mesh gauze bandage is satisfactory). A pressure bandage
should be applied if the hands are involved in the burn. The
dressing should not be disturbed for 10 days unless complications
develop.
(f) Physiological saline solution has been found useful in
the treatment of burns involving the face, hands, and especially
fingers, the flexures, and the perineum. It may also be used for
the removal,of tannic acid or other coagula previously applied
and for the treatment of sepsis. Saline may be employed in the
form of packs or baths.
(g) If for any reason as long as 2 hours must elapse before
tanning of a burn can be started, first-aid treatment should be
instituted. For burns of all surfaces except the hands, face, and
genitalia, this should consist of liberal application to the burned
surfaces of a water soluble.'jelly containing 10 percent of tannic
acid and 5 percent of sulfadiazine. If this is not available, boric
acid ointment may be substituted. The area is then covered
with a sterile dressing. First-aid treatment of burns of the
hands, face, and genitalia should consist of a liberal application
of a water soluble emulsion containing 5 percent of sulfadiazine.
Boric acid ointment may be substituted if necessary. The burn
should then be covered with a fine mesh gauze. A pressure
bandage should be applied to burns of the hands.
64
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GUIDES TO THERAPY FOR MEDICAL OFFICERS 18-19
Sec tio n III
MEDICAL EMERGENCIES
Paragraph
General_______________________________________________________ 18
Acute poisonings_______________________________________________ 19
Bites and stings_______________________________________________ 20
Poison ivy (Rhus radicans) and poison oak (Rhus diversiloba)
dermatitis___________ 21
Allergic and anaphylactic reactions_____________________________ 22
Food intoxications and poisonings______________________________ 23
Care of feet___________________________________________________ 24
Seasickness____________________________________________________ 25
Altitude sickness______________________________________________ 2G
Compressed-air illness____________________________ ._____________ 27
Electric shock_________________________________________________ 28
Immersion____________________________________________________ 29
Heat exhaustion, heat stroke, and heat cramps_________________ 30
Exhaustion___________________________________________________ 31
Starvation____________________________________________________ 32
Frostbite_____________________________________________________ 33
Sunburn______________________________________________________ 34
Acute psychoses and related conditions_________________________ 35
18. General.—As with the preceding section on surgical
emergencies, the following paragraphs cover suggestions for the
treatment of certain medical conditions that demand more or
less immediate action.
19. Acute poisonings.—a. Acids.— (1) Neutralize with an
alkali, such as magnesia, chalk, white wall plaster, sodium
bicarbonate (cooking soda), or lime water.
(2) Give a demulcent, such as milk, olive oil, or egg white.
(3) Keep the patient warm.
(4) Give 0.016 gram (*4 grain) morphine sulfate for pain.
(5) Do not pass a stomach tube or give an emetic, because
of the danger of perforation.
b. Alcohol.— (1) Acute alcoholism may be confused with a
number of other conditions, notably spontaneous or insulininduced
hypoglycemia, cerebral concussion, and acute poisonings
due to drugs, particularly cocaine (with acute cocaine poisoning,
treatment for acute alcoholism frequently results fatally).
(2) If the diagnosis of acute alcoholism is established, no
specific medical treatment is required in most cases.
(a) Put the man to bed, cover him warmly enough to prevent
chilling, and allow him to sleep until he recovers.
(b) The routine use of gastric lavage is not advisable.
65
TM 8-210
19 MEDICAL DEPARTMENT
(c) The patient should be watched until it is certain thar
the intoxication is not serious.
(c?) On his awakening, give 1.0 gram (15 grains) sodium
bicarbonate and a saline laxative by mouth, if they can be
retained; give 0.3 gram (5 grains) acetylsalicylic acid (aspirin)
by mouth for relief of general distress; if vomiting persists, give
nothing but crushed ice by mouth and administer 0.0006 gram
(1/100 grain) atropine sulfate hypodermically, repeating once
or twice at 3-hour intervals, if necessary.
(3) If the man is noisy, violent, or combative, and if he is
robust—
(a) Administer 0.006 gram (1/10 grain) apomorphine hydrochloride
hypodermically; this will nearly always quiet the
patient and will usually induce vomiting (apomorphine should
never be given to a drowsy or unconscious patient).
(b) If vomiting does not occur, a stomach tube should be
passed, and the stomach washed out with several quarts of
warm water or of a 5 percent solution of sodium bicarbonate.
(c) Barbiturates and other hypnotics should be avoided as
far as possible, and should never be given until it is certain
that a serious degree of intoxication is not. present; paraldehyde
is the safest, and may be given in doses up to 8 cc
(2 drams), best given orally in grapefruit juice with erushed
ice or rectally mixed with olive oil.
(d) In rare cases in which apomorphine is ineffective oi'
inadvisable and hypodermic administration of a sedative is
deemed necessary, inject 0.2 to 0.3 gram (3 to 5 grains) sodium
luminal or sodium amytal; these drugs are too dangerous for
general use, since their depressing effect is added to that of
the alcohol, and since they occasionally excite rather than quiet
the patient.
(4) If a very large amount of alcohol has been imbibed during
a short interval, a serious degree of intoxication may develop,
which can prove fatal from respiratory and circulatory failure,
unless energetically treated; such a condition is indicated by
drowsiness increasing rapidly to coma; dilated pupils; slow,
stertorous breathing; cyanosis; rapid, feeble pulse; loss of
reflexes; incontinence; and rarely, convulsions.
(a) Insert a stomach tube, taking extreme care that it does
not enter the- trachea, and wash ou,t the stomach thoroughly
with warm water or a 5- percent solution of sodium bicarbonate;
66
TM 8-210
GUIDES TO THERAPY FOR MEDICAL OFFICERS 19
introduce a teaspoonful of sodium bicarbonate and 30 grams (1
ounce) magnesium sulfate, dissolved in a glassful of water,
before withdrawing the tube.
(&) Take great care that the patient does not get chilled, bykeeping
him well covered with blankets and by using hot-water
bottles, if necessary.
(c) The patient should be carefully watched to prevent the
aspiration of vomitus and the attendant danger of pneumonia.
(d) Inject intravenously a solution containing 25 grams of
glucose dissolved in from 50 to 200 cc of water, together with
15 units of ordinary insulin (do not give insulin without glucose)
; this accelerates the rate of oxidation of alcohol in the
body.
(e) Make the patient breathe a mixture of 10 percent carbon
dioxide and 90 percent oxygen to stimulate respiration and
hence to increase the rate of excretion of alcohol; this is particularly
important if the respirations are depressed.
(f) If intoxication is profound, if the respirations are depressed,
and if the reflexes are abolished, give metrazol intravenously,
not exceeding a dose of 0.1 to 0.3 gram (iy2 to 5
grains). Give this slowly, taking a minute to complete the
injection; watch the patient carefully and stop the injection
if the reflexes return or if twitching of the facial muscles
appears; it is not necessary to restore consciousness.
(