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

    ﻿V\|i.35*.
    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
    TM 8-210 Wwwwwsg
    C 1! TECHNICAL MANUffi
    (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-
    2
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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.)
    3

    TM 8-210
    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.)
    TM 8-210
    C 1 TECHNICAL MANUAL
    (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.
    6
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    GUIDES TO THERAPY FOR MEDICAL OFFICERS C 1
    (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
    7
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    C 1 TECHNICAL MANUAL
    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.
    8
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    GUIDES TO THERAPY FOR MEDICAL OFFICERS C 1
    (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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    GUIDES TO THERAPY FOR MEDICAL OFFICERS C 1
    (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.
    39
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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.
    57
    TM 8-210
    C 1! TECHNICAL MANUAL
    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
    TM 8-210
    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
    TM 8-210
    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
    TM 8-210
    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.
    (