Document text
UNITED STATES ARMY
INSTITUTE FOR MIUTARY ASSISTANCE
ST31-91B
US ARMY SPECIAL FORCES
MEDICAL HANDBOOK
1 MARCH 1 9B2
SPECIAL FOBCES MEDICAL HAH
K
COrfTEHTS
Preface iji
Chapters
1 Body System 1-1 to 1-7&
Section
I - Integisentary System 1-1 to 1-7
II - Musculoskeletal System 1-8 to 1-13
III - Respiratory Systan 1-14 to 1-3*J
IV - Circulatory System 1-35 to l-iJ4
V - Digestive System 1-45 to 1^6
VI - Genitourinary System 1-57 to 1-62
VII - Nervous System 1-63 to 1-70
VIII - EtvJocrine Systan 1-71 to 1-73
IX - Eye, Ear, Nose, and Throat 1-74 to 1-78
2 Ccammic^le Diseases 2-1 to 2-46
Section
I - Parasitic 2-1 to 2-11
II - Mycotic (Fungal) 2-11 to 2-15
III - Bacterial 2-15 to 2-26
IV - Viral 2-26 to 2-33
V - Rickettsial and Spirochetal 2-33 to 2-40
VI - Venereal 2-41 to 2-46
3 Clearing Airway Cbstructions and CPB 3-1 to 3-4
4 Mental Disorders 4-1 to 4-9
5 Nutritional Diseases and Deficiencies 5-1 to 5-5
6 Pediatrics 5_1 to 6-9
7 Gynecology 7.I to 7-15
B Obstetrics g_l to 8-10
9 Orthopedics 9_1 to 9-12
10 Burns and Blast Injuries 10-1 to 10-11
n Heat and Cold Injuries 11-1 to 11-11
12 Bites (Snake, Insect, and Animal) 12-1 to 12-7
13 0/erdose and fbisoning 13_1 to 13-16
14 Nuclear, Biological, Chemical (NBC) 14-1 to 14-13
15 Shock 15.1 to 15-3
16 Emergency War Surgery 16^1 to 16-10
17 Anesthesia 17.I to T7-20
18 IV Therapy (Fluids and Electrolytes, Basics).. 16-1 to 18-2
19 Dental Emergencies and Treatment 19-1 to 19-15
20 Preventive Medicine (PH) 20-1 to 20-2]
21 Veterinary Medicine 21-1 to 21-12
22 Primitive Medicine 22-1 to 22-4
Appendixes
A Anatomical Plates A-1 to A-18
B Bacteriological and Parasitic Plates fl-1 to B-23
C Laboratory Procedures C-1 to C-5
D Cellular Ccmponents of Blood, Nomal Values, and
Significance of Blood Test D-1 to D-4
E History and Physical Examination Guide E-1 to E-2
F Field Sterilization Techniques F_1 to F-6
C crug of Choice Chart o-l to G-5
DEFACE
Ihis book is ilesigned to serve as a ready reference and review for
Special Forces (SF) njedics. It covers diseases ard medical problems that
SF medics may encounter in various areas of the world. It does not,
however, take the place or eliminate the need for a conprehensive medical
area study.
Many treatments given in this handbook umuld best be given in a
hospital where a laboratory and special equipment are available , and
personnel with serious injuries or illnesses should be evacuated to such a
if at all possible. Krww your limitations and do not exceed then,
flawnber the maxim "first thou shall do no hare" and seek the assistance of
more competent medical authority whenever possible.
Since we w»t to use as few pages as possible in presenting this
InfbTTnation , we use cotmon medical abbreviations throughout. For example,
A.
analysis
h.
-
hour
ABE
acute bacterial endocarditis
•
hanoglobin
ad
up to
HCl
—
hydrochloride
A.M.
ante meridiem
HCT
-
hematocrit
SS^I
b.i.d. -
basal body temperature
twice a day
HEEffT
—
headt eye, ear, nose &
throat
B.P.
blood pressure
Hg
-
mercury
BUH
blood urea nitrogen
h.s.
—
at bedtime
m
biological warfare
Hx
—
history
c.
Celsius, centigrade
ID
-
intradencal
CBC
complete blood count
BD
-
incise & drain
cc-
cubic centimeter
i .e.
that is
or
congestive heart failure
IM
intranuscular
CD.
centimeter
IV
intravenous
C.H.S. -
central nervous system
lU
international unit
CORD
chronic obstructive
kg.
kilogram
pulmonary disease
L.
liter
CPR
cardiopulioonary resuscitation
lab
*
laboratory
CT
clotting time
lb
—
pound(s!)
C.V.A. -
costovertebral angle;
LLQ
-
left lower quadrant
cerebrovascular accident
HCL
mid clavicular line
d.
Dic
day; dally
dilatation and curretage
Red
—
medication; medical;
medicine
DIR
deep tendon reflex
dEq .
—
ntilliequivalent
Dx
diagnosis
Dg.
—
TtilU igran
E. coli -
Escherichia coli
Hg
•
raagneslLin
e.g.
for example
MI
myocardial infarction
F.
C.I.
Fahrenheit
gastrointestinal
MIF
nerthiolate/ iodine/
formaline solution
g»
gram
nin
—
minute
gr.
grain
ml.
nilllllter
gtt.
drops
on.
milluaeter
CU
genitourinary
H.U.
•
million units
IV
Na
-
Sodlin (riatriura)
HBC
—
nuclear, biological, chenilcal
—
nasc^astric
NPN
•
nonprotein nitrogen
N.P.O.
-
nothing by mouth
-
nausea & vaulting
0.
cbjective findings
OD
overdose
oz.
—
ounce
p.
plan of treatment
p.c.
•
after meals
P.E.
•
physical exate
pH
•
hydrogen in concentration
PID
—
pelvic inflacinatory disease
PM
-
preventive medicine
P.H.I.
—
point of maximtn impulse
P.M.N.
polyroorphonoclear neutrophil
leukocytes
P.O.
-
by mouth
-
partial pressure oxygen
-
pulsus paradoxus
P.P.D.
-
purified protein derivative
ppn.
—
p»*ts per million
p.r.n.
-
as required or as needed
psi
—
pounds per square inch
PTB
primary tuberculosis
p.v.
-
through the vagina
q.
—
every
q.d.
every day
q. h.
every hours
q.i.d.
four times a day
q.s .
-
sufficient quantity
qt •
—
quart
S. - subject findings
SBE - subacute bacterial
endocarditis
sec - second
sed. - sediinentatlon
SLR - straight leg raise
sp. gr. - specific gravity
spp. • species
SO - subcutaneous
S »d S - signs and symptoms
stat. - immediately
STS - serologic test for
syphilis
Sx - syraptoras
T- - temperature
tab. - tablet
TB - tuberculosis
t.i.d. - three times a day
Tx - treatment
U. * unit
URI - upper respiratory
infection
IJ.S.P. - Lhited States Fharmacopeia
VD - venereal disease
VS - vital signs
W.B.C. - -white blood ceil, white
blood count
W.K.i;}. > 'Morld Health Og^izatlon
wo - without
wt . - -weight
SWBOL^
- increase
- decrease
- greater than
- less than
14 July 1982
Holders of ST 31-91B, Special Forces Medical Handbook,
should add to/chanye the text as follows:
IV
botton ricjht column, under SV'BOLS, add
t - i
ncrease
^ - decrease
^ - greater than
1-15
< - less than
line 2, add before or in center and right
columns
line 11 (Breath sounds ti voice}, sane as for
line 2
bottom page, 2d para from bottom under O, add
^before W.B.C. and > before 20, 00 ^
para 1-51 O. , first lino, add before B.P.
mid page, last nara before A., 2d i 3d lines,
add + sign over sliould read 89l27 & 124l:f8
oara D-4c, line 3, add
yv.B.c, ^ 4 , son
~ over should read
In addition to the above, users should be aware that
superscripts and subscriots in the text ate sometimes
out of line due to mechanical error.
CHAPTEfl 1
BODY SYSTEMS
Section I - Integmentary System
1-1. SKIM. Toii^ elastic structure covering the entire body consisting
of two layers: the epidermis and the dermis.
1-2. DIAGSOSIS OF 3FCIH DISEASES BY FHYSICAL EXAMINATJOW.
a. PriiDary lesion. Earliest changes to appe^:
(1) (tecule- Flat discolored spot of varied siae 10 mr. or
smaller .
(2) Patch. Flat discolored spot of varied size 10 Dm. or
larger.
(3) Papule. Solid elevated lesion 10 tan. or smaller.
tb> Plaque. A group of confluent papules.
(5) Module. Palpable solid lesion 5-10 tm. (may or nay not be
elevated) .
(65 Tumors. Larger nodules usually 20 ttm. or larger.
(7) Vesicle. Clrcimscribed elevated lesion 5 rm. or smaller
containing serous fluid.
<8) ftjlla. Ci rcunscr Ibed elevated lesion 5 nm, or larger.
(9) Pustule. Superficial elevated lesion containing pus.
(10) )^eal. Transient elevated lesion caused by local edema.
b. Secondary lesions result froo either evolution (natural) of the
FTimary lesions or patient manipulation of prlisary lesions.
(1) Scales. Heaped up parts of epithelitm.
(2) Crusts (Scab). Dried serum, blood, or pus.
(3) Erosion. Loss of part or all of the epidermis.
(9) Ulcer, loss of epidermis and at least part of dermis.
(5) Excoriation. Linear or hollowed-out crusted area caused by
*ratohing, rubbing, or picking.
_ . . Licbenificatlon. Thickening of the skin with accentuation
01 the skin markings.
(7) Atrophy, Thinning wrinkling of the skin resembling
Cigarette paper, ^
1-1
1-2
C0) Scar. Tne result of healing after destructicm of the
dermis .
1-3. SKIN DISOftCCRS.
a. Pruritus (Itching).
S. Compulsive itching accompanies primary Skin disease or may be
the only signs and symptorns.
O. Jiedness, uticarial papules, excoriated papules, fissures,
crusting, etc.
A. fruritus/Pruritus secondary to skin disease.
P. Correct the skin disease, or discontinue using irritating
substance, e.g., soap, clothing, chemical, etc- Use of mild
tranquilizers: Valim, Vistiral. Use of major tranquilizers: Thorazine-
Use of antihistamines: Benadryl 50 mg. t.i.d.
b. Contact denoatltis is divided into two types:
(1) Primary irritant contact dermatitis. Develops within a few
hours, reaches peak severity in 24 hours Uien disappears; caused by contact
with a chMical irritant.
(2) Allergic eczematous contact dermatitis. Has a delayed onset
of about 18 hocrs, peaks in 48-72 hours, and often lasts 2-3 weeks after
disccntinuir^ exposure to the offending antigen, (Poison ivy, o^, or
SLinac or allergy to clothing, etc.)
<3) Symptoms vary from minor itching and redness to vesicles,
redness, edema, oozing, crusting, aixl scaling; itching is usually sharply
demarcated,
(4) Remove offending agent. Use tap water, soaks, or
ccapresses. Blisters may be drained but leave the tops on. 0*al
corticosteriods - Prednisone 40-60 mg. /day x 10-14 days in severe cases.
Topical corticostericxJs are not effective in acute phase,
Antihistamines - Benadryl 50 mg. t.i.d.
1-4. BACTERIAL SKIN IlFECTIOHS.
a. Impetigo/E^thyoa. Superficial veslculopustuiar skin infection
seen chiefly In children. Ecthyma is an ulcerative form of impetigo.
S. Group A B-henolytic streptococcus Is usual cause , but
Staphylococcus aureus may be cultured also.
0. Usually affects arras, legs, and face, with the legs being
more susceptible to ecthyma than unexposed areas. Both (nay follow
superficial trauta or may be secondary to skin disease or insect bites, biA
it is not uncomon for it to arise on normal skin.
Lesions vary from pea-sized vesicopustules to large bizarre
circinate rir^wormlike lesions that progress rapidly from maculopapules to
vesicopustules or bullae to exudative end then to heavily crusted circinate
lesions. Ecthyma is characterized by small, purulent, shallow ulcers
covered with crusts. Itching is cooinon and scratching can spread the
infection .
A. Inpetigo/ecthyrea.
P- Systemic antibiotics are superior to topical antibiotics.
Penicillin is the drug of choice; second choice is erythrcnycin.
IH Penicillin ORAL Penicillin Erythrcmycln
Child 600,000 U. Pen G 125 tng. q.l.d. x 10 days 125 eng. q.i.d. x 10 days
Adult 1.2 mil 1). Pen C 250 rug. q.i.d. x 10 days 250 mg. q.i.d. x 10 days
In secondary impetigo, the urtderlying cause should be treated also,
Neglected infection nay result in cellulitis, lynphangitis, or furunculosis in
adults or acute glcfnerulonephritis in children.
b. Erysipelas. A superficial cellulitis caused by Group A
B-hemolytic streptococci.
S. The face (bilaterally) , an arm, or a leg is oiost often
involved.
O. Lesion is well demarcated, shiny, red, edematous, and tender;
vesicles and bullae often develop. Patches of peripheral redness arid
regional limphadenopathy are seen occasionally; high fever, chills, and
malaise are comon. It nay be recurrent and nay result in chronic
lymphedema. The causative agent may be difficult to culture from the
lesion, but it may be cultured from the blood.
A. Erysipelas. NOTE : Erysipelas of the face isust be
differentiated from herpes zoster; contact deriEatitis and angioneurotic
edema may also be mistaken for erysipelas.
P. Pen VK or erythranycln 250 mg. q.i.d. x 14 days. In acute
cases Pen G 1.2 reilllon U. IV q.bh. x 36-48 hrs then start F^n YK. Local
disconfort nay be relieved by cold packs and/or 600 rg. aspirin with 30 (Hg.
codeine.
e. Cellulitis. Has the sane S and S and is treated the sane as
erysipelas. The only difference is cellulitis involves deeper tissue.
d. See (Jiapter 2, Section III, Bacterial, for typhoid fever, gas
gangrene, anthrax, tularemia, plague, leprosy, and scarlet fever.
1-5- SUPERFICIAL FLWGAL INFECTIOKS.
a. See Chapter 2, Section II, Mycotic, for coccidloidcaycosls , North
Anwican blastcnycosis , and Paracoccidioidcmycosis (South American
bla^^omycosi s) .
Sporotrichosis. A chronic fX^tgal infection caused by Sporothrix
^chenckii. It is found worldwide in soil, plants, and decaying wood,
ganian is introduced by skin trauna, usually on hand, anc, or foot.
S. and 0. CcrnBonly begins with a hard, nontender subcutaneous
"Odule that later becemes adherent to the overlying skin, ulcerates
(cnancrifom) , and (xay persist for a long time. Witnin a few days to
1-1
1-4
weeks, sLralLar modules usually develop along tte lymphatics draining this
area, and these may ulcerate. The l>«phatic vessels become irdurated and
are easily palpable. Infection usually ceases to spread before the
regional lymph iDodes are invaded, and blood-bone disseininatiori is rare.
Skin infection may not spread through the Ijmphatics but n\ay
appear only as warty or papular scaly lesions that nay beccne pustular.
Mssaninated sporotrichosis presents as multiple, hard subcutaneous modules
scattered over the body. These become soft but rarely rupture
spontaneously. Lesions may also develop in bones, Joints, muscles, and
viscera .
Laboratory findings: Cultures are needed to establish diagnosis.
A. Sporotrichosis.
P. Saturated solution of potassiun iodine (S.S-K.I.) 5 drops
in a glass of water t.i.d., after meals, orally, increasing by 1 drop per
dose until 40 drops t.i.d. are being given. Continue until signs of active
disease have disappeared. Then decrease the dosage by 1 drop per dose
until 5 drops per dose are being given, then discontinue. Although
S.S.K.I. is not fungicidal, it does promote rapid healing. Ca-e must be
taken to reduce the dosage if signs of iodisn appear.
Amphotericin B IV and miecnazole have been effective in systaiic
infections.
c- ChromcBiycosis. Mainly a tropical chronic cutaneous infection
caused by several species of closely related teolds having a dark nycelii®.
Found in soil and on decaying vegetation. In hifoans the disease progresses
slowly, occurring most frequently on the lower extremities, but it may
occur on hands, arms, and elsewhere.
S. and 0. Lesions begin as a papule or ulcer. Over a period
of TDonths to years, the lesions enlarge to become vegetating,
papillomatous, verrucous, elevated nodules with a caiiliflowerlike
appearance or widespread dry verrucous plaques. The latter spread
peripherally with a raised, verrucous border, leaving central atrophic
scarring. The surface of the border contains minute abscesses. Satellite
lesions may appear along the 1 juiphatics . There nay be a foul odor due to
secondary bacterial Lnfecticn. Some patients complain of itching.
Elephantiasis may result if marked fibrosis and lymph stasis exist in the
limb.
Lab findings: The fungus is seen as brown, thick-walled,
spherical, sometiries septate cells in pus.
A. QircfDcmycosis.
P. Flucytosine - 150 mg./kg./d. orally or thiabendazole 25
mg./kg./d. orally. Surgical excision and skin grafting may prove useful.
d. Eermatophyte infections (Ringworm) , Superficial infections
caused by fungi that invade only dead tissues of the skin or its appendages
(stratum comeun, nails, hair).
S. KLcrosporun , Trichophyton , and Epidemophyton are the gwiera
Eost cowionly involved.
0. Some deiTnatophytes jx-oduce only mild or no inflamnation. In
such cases, the org»]ism may persist indefinitely, causing Lntennittcit
remissions and exacerbations of a gradually extending lesion with a
scaling, slightly raised border. In other cases, an acute infection may
oco^F typically causir^ a sudden vesicular bullous disease of the feet,
or an inflamed boggy lesion of the scalp (Xerion) may occur that is due to
a strong iwmjnolcgic reaction to the fungus; it is usually followed by
remission or cure,
A. Tinea corporis - (Ringwonn of the body).
Tinea pedis - (Ring>*orm of the feet) - athlete's foot.
Tinea ur^uiun - (Ringworm of the nails).
Tinea capitis - (Ringwonn of the scalp) - dandruff.
Tinea cruris - (Ringworm of the groin) - jock itch.
Tinea barbae - (Ringworm of the beard area).
Tinea mamium - (Ringworm of the palms and soles of the
feet).
Differential diagnosis; Includes pityriasis rosea, discoid
eczema, and psoriasis.
Confirmation c» be rr«de with Wood's light or KOH
preparation .
P. Griseofulvin is effective against true dermatophyte
i^f®ctions, but not against candidiasis or tinea versicolor. Adult dosage
is 5tX) mg. b.i.d. with meals. Duration varies from 2 weeks for tinea
corporis to 6-12 months for tinea ur^uium. Tinactin/Hycostatin are
effective against most fuigal infections where applied b.i.d. to t.i.d. to
affected areas and washed off before reaj^lication .
1-6. PARASniC SKIM INFECTIOHS.
a. Scabies. A tr^sBisslble parasitic skin infectiwi characterized
by superficial bierowB, intense pruritus, and secondary Infections.
S. Caused by the itch mite (Sarcoptes scabiei). The female mite
tunnels into the epidermis layer and deposits her eggs along the burrow.
Rabies is transnitted by skin-to-skin contact with an infected person. It
not traranitted by clothing or b6<3dijig*
O. nocturnal itching, pruritic vesicles and pustules in ’•ruis'*
or ’’galleries" especially on the sides of the fingers and the heel of the
palms. Mites, ova, and black clots of feces may be visible
Bu-croscopically .
Scabies. Confirm by demonstrating the parasite in scrapings
From a burrow, mix with any clear fluid, and examine microscopically.
P. Disinfestation with gama Kwell 1| cream base applied from
neck dom and repeated in one week. (WARNDIG: there is a potential of
neurotoxicity from use on infants and from overuse on adults.) Treatment
1-5
1-6
^uld be aimed at all infected personnel. In cases of ^vere secondary
infections, treatment ^uld be supplauet ted with systemic and topical
antibiotics.
b. Pediculosis (Lice). A parasitic infestation of the skin— scalp,
trink, or pubic areas— that usually occurs in overcrowded dwellings.
S. Head and pubic lice can be found on the bead and in the pubic
area. Body lice are seldOD foieid mi the body as the insects only ccme to
the skin to feed; you must look for them in the scans of clothing.
O. Pruritis with cjceoriation, nits (ova) on hair shafts, lice on
skin or clothing, occasionally sky-blue macules {naculM ca^uieae) on the
inner thighs or on the lower abdomen in pi*ic lice Infestations. You nay
also see secondary infections,
A. Pediculosis pubis (Crabs - Phthlrus pubis). Infestation of
»ogenital region. Pediculosis hoi£fiu&-var corporis (body louse).
Differential diagnosis seborrheic dermatitis, scabies, anogenital pruritis,
and eciena.
P. Cure is rapid with garma Xuell It q,d. x 2 days. Repeat
after 10 days to destroy the nits; practice good personal hygiene. If the
infestation is widespread, wash all clothing and bedding in hot water with
a strong detergent and dust the area with lindane powder.
c. See Chapter 2, Section 1, Parasitic, for African trypanosomiasis
(sleeping sickness), jtoerican trypanosaniasis tCS^agas' disease), and
cutaneous and mucocutaneous lelshcDaniasis .
1-7. VIRAL ItFECTIOMS OF THE SKIN.
a. Herpes simplex (cold/fever sore). An acute viral infection.
S. Clinical outbreaks, which may be recurrent in the sa»e
location for years, are provoked by fever, siffiburn, indigestion, fatigue,
windburn, menstruation, or nervous tension -
O. Etecurrent, small, grouped vesicles on an -erythematous base,
especially around the oral and genital area, lasting approximately 1-2
weeks . Regional lymph nodes nay be swollen and tender . Burning and
stinging; neuralgia nay precede and accompany attacks. The lesions consist
of small, grouped vesicles that may occur siywhere, but most often occur on
the lips, rrcuth, and genitals.
A- Herpes simplex. Differential diagnosis: Distinguish from
other vesicular lesions, especially herpes zoster and impetigo, in the
genital area, syphilis, lymphogranuloma venereim, arid chancroid.
CDMPLICATIOMS: Xaposi's varicelliform eruptions (eczema herpeticixn or
disseminated herpes simplex), encephalitis, keratitis, and perhaps cervical
cancer and other neoplastic diseases.
P, Diminate precipitating agents when possible. Apply a
rwistened styptic pencil several times daily to abort lesions. Dust
vesicles twice daily with bismuth formic iodide or use shake lotions or
caxphor spirit. Epinephrine 1:1,000 applied locally b.i.d. may also be
used. If there is associated cellulitis and lymphadenitis, apply cool
c^copresses . Treat stcmatitis with mild saline mouthwash.
b. Herpes zoster (Shingles). An acute vesicular eruption due to a
virus that is morphologically identical with the varicella virus.
S. Usually cKcurs in adults with or without a history of
chlckenpox during childhood and is probably a reactivation of a varicella
virus infection that has been occult for many years. Persons in anergic
states (Hodgkin's disease, Ij^nphomas, or those taking inmunosuppressive
dr^gs) are at greater risk, and li fe-threatcniog dissemination (varicella)
may occtr-
O. Pain along the course of a nerve followed by painful groups
of vesicular lesions. InvolveiBent is milateral and persists for
approximately 2-3 weeks. Lesions are usually on the face and trunk.
Swelling of regional lymph nodes may occur. Pair usually precedes
^uptlons by ^ hours or more and may persist and actually increase in
intensity after the lesions have disappeared.
A, Herpes zoster. Differential diagnosis; ftjison ivy, poison
oak dermatitis, and herpes simplex, which is usually less painful.
CONFLICATIONS: Persistent neuralgia, anesthesia of the affected area
following healing, facial or other nerve paralysis, aid encef^ialitis may
occur .
P. Barbitirates nay help control tension and nervousness
associated with neuralgia. Aspirin with or wit)»ut codeine <30 mg.)
usually controls the pain. A Single injection of triartKinolone acetonide
(Kenalog) suspension (kO nig. intragluteally) may give prcoipt relief.
Prednisone AO njg. daily for A days and then -continued in declining doses
may also be used. Calamine lotion or other shake lotions are often of
value; apply liberally and cover with a protective layer of cotton. CO HOT
USE GBEASES .
c. See Chapter 2, Section IV, Viral, for measles, smallpox, dengue,
Colorado tick fever, and herpes genitalis.
d. See Chapter 6, Pediatrics, for chickenpox.
1-8- RICKETTSIAL DISEASES. See Chapter 2, Section V, Rickettsial and
Spirochetal, for epidemic louse-borne typhus, endemic flea-bome typhus,
and spotted fevers (Rocky Mountain spotted fever, Rickettsialpox, scrub
typhus, trench fever, Q fever).
1-9. SPIROCHETAL DISEASES-
a. See Chapter 2, Section VI, Venereal for syphilis.
See Chapter 2, Section V, Rickettsial and Spirochetal, for
treponwal infections (yaws, endmic syphilis, pinta).
1-7
1-8
Section II - (tisculoskeletal System
1-10. GENERAL.
a. The history of a musculoskeletal disorder is aijch like any other
history- A cjoncise story of specific coroplaiats will help the leedic best
determine the extent of the disorder. Questions should include
chronological sequence, manner of onset, duration of symptoms, previous
history, progress of the complaint, extent of disability, specific
ccmplaint of weight bearing, Tnotion of the part, weather changes, what
aggravates the complaint, relieves it, whether it has ever been
treated, and if so, what were the effects of treatment.
b- The physical examination Should include the general posture and
augment of the body as a whole. Evaluate the patient's body attitude
viiile standing and walking. The relationship of the feet to the legs and
of the hips to the pelvis should be noted; also the relationship of the
.^Tus to the shoulder girdle and to the upper trunk. Next the general
contour of the spine and its relation to the shoulder girdle, thorax, wi
pelvis should be noted, the local physical examination should include:
(1) Inspection. Contour, appearance, color, deformity, and its
general relationship to the body.
(2) Palpation. Tenderness, swelling, muscle spaaa, local
temperature changes, and gross alterations.
(3) R£«ge of motion, tttion is measured in degrees of a circle
as illustrated below. Medic should compare affected area with ^involved
opposites or with his own joints.
(U) Joint position. Position of ftrvction is the position that
gives the Joint its maximijii strength and efficiency. Position of ccmfort
is the position in which the joint feels the most ccmfortable. Patients
will always try to assune the position of ccmfort. It is up to the medic
to insure that the affected joints are always supported In a position of
function .
(5) Measurement. Atrophy or hypertrophy may be determined by
measuring and comparing with ininvolved opposite.
(6) neurologic- The strength of the affected muscles and the
qLtallty of the superficial and deep tendon reflexes should be noted- Also
the integrity of cutaneous sensation should be determined when indicated.
Vll. RHEUMATOID ARTHRITIS. Chronic systemic disease of unknown etiology
' usually involving the synovial tnembranes of multiple joints, tendons, or
bursae.
S. and 0. Common in ages 25-50; women are affected three tines as
often as men. Abrupt onset with sjranetrical swelling of joints in the
hands and feet, regional atrophy of bone and muscle, lioited joint motion,
the skin of the extremities may be sncoth, glossy, and atrophic. Other
signs and symptons Include elevated temperature, tachycardia, generalized
lycnphadenopathy, malnutrition, body wastir^, oorhing stiffness, and
depression. Synovial fluid is cloudy and sterile, reduced viscosity.
Polymorphonuclear leukocytes typically predominate. History should rule
out other types of arthritis.
A. f^urnatoid arthritis.
P. Rest, aspirin in high doses (look out for ulcer), corticosteroids,
either systemically and/or intra-articular injection. Severe rebound may
follow steroid withdrawal. Heat and physical therapy to maintain joint
function .
1-12. C6TE0AHTHRITIS. A degenerative Joint disease usually affecting
large weight-bearing joints of older individuals, causing deterioration of
articular cartilage.
S. and 0. Onset is gradual and localized to a few joints; 60-70-
year age bracket; vrcmen affected 10 times as often as men; distal
Interphalangeal joints of the fingers frequently show modulation, obesity;
pain is made worse by exercise. The cervical and lutibar spine, hip, and
taee are most often involved. History, physical, laboratory findings will
show minimal abnomalltles.
A, Osteoarthritis .
P. Best, weight reduction, heat, occasional brace support,
aspirin, analgesics, and physical therapy.
^-13. SEPTIC ARTHRITIS. ^ Acute disease process involving a single joint
and is secondary to a bacterial infection.
S. and 0. JVeviously healthy, case of gonorrhea usielly in
women, concurrent bacterial infection, fever, rash possibly, acute joint
pain and stiffness, joint is warm, tender, swollen- Leukocytosis,
arthrocentesis will show color to be variable, viscosity variable, clarity
opaque, culture often positive. Gran’s stain, W.B.C. greater than 10,000.
A. Septic arthritis.
P. Evacuate if possible; the joint may be destroyed if not
promptly treated. Treat with antibiotics according to infectious organism.
1-iy, QCKJTY ARTHRITIS. Recurrent metabolic disease usually ca^jsing
arthritis in perifdverial joints due to hyperuricemia that leaves irate
crystals within the joint space.
I -9
1-10
S. aod 0. Minor trauma raay start; overindulgei>ce in pork or
alcotol; classically the joint of the tig toe is affected; innaraation,
pain, swelling, fever, chills, tachycardia; urate salts nay precipitate in
a collection called a tophus that rnay be mistakenly reported as
calcification. These tophi may be found in the muscle surrounding the
joint, the tendons, or the walls of the bursae. Usually made by history
artd physical. Synovial fluid will have needle-shaped urate crystals that
are free in the fluid.
A. Gouty arthritis,
P. Teminate the acute attacks by the use of »
anti-inflamatory drug, prophylaxis by daily use of colchicine, and
prevention of further deposits of urate crystals by lowwing uric acid
levels with Benemid cr sQlopurinol. Codeine nay be needed to control pain.
1-15. OSTEOMYELITIS. An infection of the bone and bone marrow die to
septicemia or bacteremia.
S. and 0, Infected tonsils, bolls, abscessed teeth, or upper
respiratory infections may cause the septicemia. Direct contmination may
result from open fracture or war woutkI. General symptoms are those of an
acute toxic illness with sharp rise in temperature. Locally the involved
area may be swollen, warm, and very tender to touch. There may be a
severe, constant, pulsating pain, usually aggravated by notion. The
diagnosis of acute osteomyelitis ideally requires the identification of the
causative agent. Staphylococcus aureus is the most cofrmon, accounting for
65-70 percent of the cases. Proteus, pseudomonas, salmonella,
streptococcus, acid-fast bacilli, fungi, aid rickettsiae can also be the
cause. Blood test will usually show an elevated leukocyte count and blood
culture may be positive.
A. Cstecmyelitis.
P. The successful treatment is canpLetely dependent upon
establi^ing an early clinical and bacterial diagnosis. Antibiotics are
started as soon as diagnosis is suspected and may be altered after the
results of the culture and sensitivity are known. Penicillin G with doses
of 12-20 million ursits daily and 1-6 grass of methiclllin dally, depending
on patient’s age. For patients that are allergic to penicillin,
cephalosporin, erythromycin , or lincomycir reay be given. Antibiotics
should be contintted for 8-12 weeks after all signs and symptoms disappear.
The affected bone should be inmobilized until all signs of active, infection
have disappesred. Aspiration of abscess nay also be necessa-y. Chronic
osteomyelitis recfuires surgery with radical debridement of the bone with
excision of all sinuses, dead bone, scar tissue, and necrotic tissue.
1-16. BURSITIS, Inflamraation of the bursa. Bursae are lubricating
devices that diminish the friction of movement. They are found beneath the
skin, beneath tendons, and overlying joints. Inflammation may be due to
traima, extensive use, infection, gout, or rheumatoid arthritis. Due to
the stimulus of inflafomation , the lining manbrane produces excess fluid
causing distension of the bursa sac. The fluid may be bloody or in the
case of gout, there may be urate crystals. Treatment consists of local
injections of corticosteroids into the infiamned bursa. Treatment of
choice is 20-*i0 mg. hydrocortisone following infiltration of It procaine.
Phenylbutazone 3C0 mg. for 2-3 days followed by 100 mg. for 10 days is also
effective. Early active movement inhibits development of limiting
adhesions.
1_17. ARTHROCETfrESIS. Find the effusion. Hark the site for entry. Scrib
nith Betadine or iodine. Anesthetize the skin It lidocaine. Aspirate with
20-gage needle; insure needle is long enough. Record the voline,
' viscosity, color, and clarity of synovial fluid. Inmediately place 0.5 mi.
in sterile tube for culture with Thayes-Martin nediLrn. Place 0-5 ml. of
synovial fluid in a heparinized tube for leukocyte count. Use 0.3S saline
solution as diluent for W.B.C. Prepare smears for Wright's and Gran's
stain. Prepare wet SR>ear by placing drop of synovial fluid on slide, cover
with cover slip, and seal edges with nail polish.
SHOLLDER. Shoulder pain may arise frca a problea primarily in
Joint or it may be referred pain. Referred pain may be due to cervical
Spine disorders, cardiac disorders, gallbladder diseases, or diseases
^volving the nediastinun or diapbr^m. Referred pain will less likely
have local tenderness, inflauination , and limited range of motion.
1-11
1-12
Sternoclavicular
1-19. THE KNEE-
a. Collateral liganent nature test. With tlie knee partially flexed,
an abnormal opening of the medial aspect of the knee indicates damage to
the medial collateral ligament. If the lateral collateral ligament has
been injured there will be an opening on the lateral aspect of the knee-
b- Cruciate ligament rupture test. With both knees flexed^ the medic
grasps the leg just below the knee with both hands and pulls the tibia
forierd. For best results the medic should place his hip on the patient's *
foot. Abnormal forward motion of the tibia suggest damage to the anterior
cruciate ligaments. Abnormal backward notion of the tibia suggests damage
to the posterior cruciate ligaments.
c. rtzMurray's test for torn meniscus. The patient should be lying in •
the supine position with the knee fully flexed. The foot is forcibly ’
rotated outward to Its full capacity. Wille the foot is held outward in •
the rotated position, the knee is slowly extended. If a painful click is
felt, this indicates a tear of the medial meniscus. If the painful click
is felt when the foot is rotated inward, the tear is in the lateral
mwiiscus.
1-20. LOW BACK PAIN. A thorough knowledge of the anatomy of the spine,
particularly of the limbosacral area, is essential to the diagnosis and
treatosent of low back pain. Low back pain may be due to congenital
disorders, tuawrs, tratma , metabolic disorders, inflamatory diseases,
degenerative diseases, infections, mechanical causes, or psychoneurotic
disorders. This does not end the list. Trauna is the most coranon cause of
back pain. A study of the presented disorders will help the medic in his
differential diagnosis. General treatment consists of bed rest, beating
I
pads, firm mattress, massage, and possibly a local anesthetic infiltration
to trigger points.
a. The malingerer. Malingerers exist, but every patient should be
treated as a true patient intiL other evidence exists.
h. The tests-
n? Have the patient sit in a chair and try to touch the floor;
a patient with a severe disc herniation can usually perfom while the
malingerer cannot.
{2) Place the patient in the supine position. Put one hand
under the heel and raise the opposite leg. A nalingerer will usually lift
his heel cut of the medic's hand liiile the legitimate patient will press
further into the hand.
(3> The malingering patient usually exhibits a marked withdrawal
response when the medic palpates any part of his bcdy. Squeezing the
sacroiliac joints by ccmpression from both sides usually elicits pain from
the patient who is faking and not fron the true patient .
U) Hjscle weakness in the injured side is usually too obvious
and disproportionate to the neurolcgical findings in the malingerer. The
best course of action is to tell the patient that no organic cause can be
found for the patient's symptcns.
1-13
1-R
Section III - Respiratory Systew
The respiratory system includes the nasal pharynit, sinuses, trachea,
Dronchial tree, Imgs, pleura, diap^iran, and the chest wall-
The upper portion of the respiratory systea is covered in Chapter 1,
Section IK, EENT.
t-21. PNEUMOTHORAX: The presence of air in the pleural cavity resulting
in partial or total collapse of the lung.
5. Closed pneunothorax : No direct conmunlcatlon between pleural
cavity and the atmosf^re.
fO Spontaneous pneunothorax: Due to rupture of a bleb at
the surface of the lung lining. Most ccnnon in otherwise healthy males
between 20-30 years of age. Sudden onset of progressive dyspnea is the
oost corotBon complaint. Qiest pain of variable quality (but usually
pleuritic) is frequently associated- The rupture oftw occurs during
exercise, coughing, sneezing, or straining, and the patient can usually
pinpoint the onset of dyspnea to the second. The progression is usually
rapid, and the patient may find himself in severe respiratory distress in
Minutes. The course, however, may be less acute and the patient may note
only slowly increasing dyspnea on exertion for days prior to onset of frank
dyspnea at rest. The chest pain is usually localized to the affected side.
12) Tension pneLinolhorax : Due to rupture of a small
bronchus, bronchiole, or alveolus- This results in the formation of a
one-way valve that allows inspired air to enter but prev^ts its escape.
The progressive increase in pressure frcm the trapped air builditp pushes
the heart to the opposite side and ccxcpresses the uiivalved lung and great
veins resulting in a decreased cardiac output. The symptoms are the same
as spontaneous pneunothorax but far raore rapid in progression. The chest
pain usually localizes well to the affected side, initially, but may beccne
more diffuse as the ccntralateral lung is involved.
D. General: The patient is usually anxious and tachypneic.
Signs of varying degrees of shock may be present depending on the type and
extent of the pneunothorax. The sar&e car be said for cyanosis.
Vital Signs: Ten^wrature is usually normal but may be subnormal
if severe degree of shock is present. Pulse is usually increased and
feeble. Respiration is tachypneic.
B.P.: A postural drop may be noted with significant
cardicwascular coraprorai se ; a persistently low or falling supine B.P. will
be seen as shock becomes more developed.
Ches t Exam:
Chest expansion
[esonarce
percussion
Breath sounds & voice
sounds
Fremitus
Tracheal deviation
TMTTTshT
Tracheal A P.W.T. *’swir^"
(a pefxluliiD type motion
of the heart 4 trachea
during expiration and
inspiration is often
seen in pnetnothorax) .
Spontaneous
or absent o<
side .
Involved side>uninvolved
side
or absent on involved
side
Absent
Usually none
Usually none
Insp: Toward involved
side
Expir: Away from
Involved side
Tension or Open
or alisentr on
affected side
greater than
uninvolved side
C^ich may also
demonstrate poor
expansion)
Involved side>
uninvolved side
or absent on
involved side
Absent
When present, is
away from
affected side.
When present, is
away from
affected side.
Insp: Away
from involved
side
Exp: Toward in-
volved side
Subcutaieous atiphysema : Air in the subcutaneous tissues about
the neck and chest usually indicates an underlying pneunothorax.
A. Pneunothorax. Differential diagnosis: Hay mimic many acute
thoraxic events including pulmonary embolus and MI. The specific features
of denonstr^le hyperresonance with associated poor expansion of one side
of the chest will usually differentiate a pneunothorax. Nonetheless, a
quick rule of other possible causes should be done.
P. Closed preurothorax :
(1) Spontaneous - Tube thoracostomy with drainage:
(a) At the 3rd or Mth intercostal space j\ct medial to
the anterior axillary line, make a short skin incision just above and
roughly parallel to the inferior rib of the interspace.
(b) Use large hemostats to separate the muscles and
ptMicture the pleura.
(e) With the hemostats, introduce a large bore Foley
catheter into the pleural space with the tip pointing superiorly (if a
chest tube is available, use it).
(d> Tiw tube should be inserted 1/2 to 3/^ of its
length and the balloon inflated. The catheter is then slowly pulled
outward uitil the inflated balloon "catches" on the inner chest wall-
During this time the patient should be urged to cough and strain to allow
roBoval of pleural fluid. Chce the catheter catches, it Is secured with
sutures. A vertical mattress suture wrapped around the tube is preferred.
1-15
1-16
The wcumd, tDo» is "tighter>ed’' with sutures, and petroletm gauze overlaid
with dry dressing is placed over the entrance. Secure the edges of the
dressing out to 6 inches with tape, ti^tly . DO MCT secure with
circimferential wraps around the chestT
(e) If the tube does not have a one-way valve, ore can
be improvised by tying a finger cot, a finger cut out of a rubber glove, or
a condcai over the end of the tube and cutting a scsall hole in it. A rubber
Penrose drain slipped over the end (with a few centi8)eters "left dangling’')
will accomplish the sane (i.e., prevent air reflux into the chest). The
water bowl seal can be used for the same pxrpose. See illustrations below.
Vater bowl seal bowl must be kept below level of patient.
Penrose drain
Improvised one-way valve.
(f) If a water seal device is available or can be
improvised, it is preferable. A simple 2-bottle water trap suction system
is illustrated below.
Two-bottle water seal trap for pneumothorax.
(2) Tension Pneifoothorax: Because of the rapid progression
of derangefBents and their ocaisequences (i.e., shock), heroic steps may have
to be taken to buy time for tube placement and definitive management.
(a) If a tension pneiiBOthorax is suspected and the
patient is cyanotic or manifests any signs of cardiovascular compromise
(e. g., postural drop in B.P., fraik hypotension; cold, clammy skin, etc.),
a #18 or #16 needle should be introduced into the chest to decompress the
pleural space. The needle should be introduced slowly in the 2d or 3rd
intercostal space HCL until the '’hiss" of air can be heard (...get your ear
doMi there and listen!!) escaping. Avoid the underside of the superior rib
(see 1-27, Pleural Effusions).
(b) When the Initial blast of air ceases, remove the
needle and institute tube thoracostomy and drainage as outlined above.
(3) General care after closed thoracostomy - tube drainage:
(a) Monitor patient for signs of continued improvement
(or deterioration). Have the petient cough occasionally, and check ftw
signs of air movement in the tube or water trap system. If patient exan is
consistent with sustained expansion and no air leak is noted for 24 hours,
the tube may be clamped. In an unccmplicated spcmtaneous pneunothorax , the
tube may be withdrawn after another 24 hoirs of continued stability. The
mattress suture is drawn tight and closure effected as the tube is pulled
clear. Pulling the tube in the field Is, however, strongly discouraged in
spontaneous pneumothorax and absolutely contraindicated in open or tension
pneijnotborax .
^h) If the pneimothorax persists with evidence of good
(large leak into the pleural space) or without evidence of
good air drainage (obstructed or poorly positioned tube) a second tube
1-17
1-18
should be placed nearby to facilitate drainage. If a ai^ificant
hen»thorax is present (open chest trauea, etc.) a second tube should be
placed in the 6th or 7th intercostal space in the mid or posterior axillary
line. The presence of fluid there should first be confirmed by needle
aspiration.
<c) Tetanus prophylaxis is given and all drainage
routinely Gram-stained for evidence of infection.
1-22. ASPIRATION.
a. Definition: Inspiratory sucking into the airways of fluid or
other foreign material. Two types:
(1) Active aspiration: The patient's airway defense mechanisms
(coughs gag, etc.) are overwhelmed by the sudden collection of matter in
the posterior pharynx. This usually happens as a result of ycaniting but
car happen with rapid hemorrhage that drains into the area (i .e. , maxillo
facial trauma, severe hose bleeds) . Crowning is also a type of active
aspiration .
(2) Passive aspiration: Cropharyngeal secretions pool in the
posterior pharynx and passively "leak" into the trachea. Almost always
occurs in the presence of sli^ish or absent airway defense tiiecbanisms
(obtundation, ccoa, etc.).
b. Pathology. Three major events nay occia-:
(1) Asphyxiation (’'strangling'*): Ccctrs 'when large voluoes are
aspirated resulting in extensive airway obstruction.
<2) Aspiration pneunonia: Occurs as a result of aspirating
oropharyngeal secretions that contain numerous potentially pathoiogicai
organiatis .
(3) Chemical pneinonitis: Say result from aspiration of highly
acid stomach secretions. It is a type of noncardiac pulmonary edena.
S. The actual event (vomiting, choking, etc.) may have been
witnessed, but it is likely that the victim of active aspiration will be
found cyanotic "and in severe respiratory distress. The usual history of
passive aspiration is the onset of fever and progressive respiratory
distress after or during a bout of obtundation.
Any recent Hx of obtundation in a patient with respiratory
distress should alert the examiner for aspiration. Any Hx of conditions
that may produce unconclousness (alcoholiai, seizure disorder) has the sane
significance.
0. General appearance: With massive aspiration, vomitus or
other matter may be seen about the nose and mouth. Ihe patient may be
cyanotic with varying states of conciousness (ranging from alert to fraik
ccna) depending on degree of obstruction, time obstruction present, and
nature of associated injiries.
VS: TemperatLre may be elevated if pneuncnia or chemical
roei«>nitis has developed. Pulse is usually increased. R. is usually
^creased and labored. B.P. may be decreased or may exhibit postural drop
if shock is present or imminent.
Asphyxiation Pneinonia Pneumonitis
Heck Use of accessory muscles Use of Use of
may be prominent until accessory accessory
near the end. muscles muscles.
unusual or
until advanced
stages .
Resembles The findings
findings in of pulnwnary
other edema (rales,
pnetruonias rhotKhi,
(i.e., signs wheezing,
of ccrsol- etc.) .
idation) ,
Lab: W.B.C.: Hay have leukocytosis with left shift, especially if
pnetxnonia is present.
Sputum exam: Many W.B.C. ; mixed flora.
A. The most important clue to diagnosis is the presence in the
Hk of a suspect setting .
P, (1) Clear the airway by maiual extraction of foreign matter.
Use suction if available. The Heimlich maneuver may be necessary to clear
the airway.
(2) If patient Is conscious and can cough, administer regular
chest percussion and drainage. If the patient is utKonscious , he should be
intubated amd secretions renwved by suction .
(3) Med: Oxygen, if avail^le, should be administered.
Antibiotics are the preferred methods: Tobranycln or gentareycin BO mg. IV
or IH b.i.d.; Penicillin C two million units IV q.6h. Brotxihodilators may
be of benefit- Aminophyllioe (as per asthma).
c. General considerations. The best trea'tmenb is prevention.
Severely debilitated or obtunded patients should not have food or liquids
"forced'* upon them. Their heads should be kept at a 3CM150 angle. If a
patient has no gag reflex, carnot cough or gargle a small amount of water
without choking, he should be considered a high risk for aspiration. Wet,
gurgling noises on inspiration and expiration may represent impending
passive aspiration in the obtunded patient. He should be inmediately
Auctioned or his airway evacuated by postiwal methods.
1-23. HEMOPTYSIS, Spitting or coughing up blood of respiratory tract
. Massive hemoptysis: hemorrhage exceeds 200 cc. in 24-hr period.
a. Pathology: The bleeding may come free a lesion anywhere in the
respiratory tract. Hemoptysis can be deadly. Few patients "bleed to
death;" rather death is almost always due to aspiration asphyxiation U.e.,
1-19
Liangs Poor breath sound over
large areas may be noted;
coarse rhonchi .
1-20
they "drowi" in their own blood) -
b. Causes: Lung abscess/TB/scoK he^t diseases {mitral
stenosis)/crushing , penetrating or concussive chest traiina/penetratirig neck
injuries.
S. Questic»i for evidence of disease states outlined above.
Trama should be obvious .
O. General appearance: Search for signs of possible respiratory
collapse {cyanosis, lethargy, etc.). In severe states, use of neck
accessory muscles and retractions of the chest nay be seen. Dullness and
poor expansion nay be noted on the side where bleeding is originating {if
eoTiing frcoi a luig). Rhonchi, rales, and wheezes may be heard. Decreased
or absent breath sounds may be heard over the side most Involved.
A. Hemoptysis should be obvious, but take care to distinguish
from G. I. bleeding.
P. (1) Clear the airway. Chest percussion and drain^e. If
the bleeding is too brisk or the patient is in severe respiratory distress,
intubation should be carried out with vigorous suction. Do not intubate if
suction not available unless the patient is unconscious.
( 2 ) Massive hemoptysis or anv hemoptysis associated with
severe respiratory distress is an emergency that cannot be adequately
managed in the field. Evacuate ASAP!! The measures outlined above are
temporary supportive measures only.
FWELIMONIA. An inflanaation of the Itng parenchyma to include the
aveoli and analler airways. Though the inflMmation nay be secondary to
any niDber of processes, the term as used in this discussion will apply to
infectious processes.
a. Bacterial pneumonia. An acute infection of the alveola* spaces
of the lung. Organisns causing pneunonia include pneuDococci,
staphylococci , Croup A hemolytic streptococci. Klebsiella pneuncnia,
Haemophilus influenzae, and Francisella tularensis.
(1) fhieuBococcal pneuronia. The pneunococcus accounts for 60-80
percent of primary bacterial pneunonia. Among conditions which predispose
to pneumonia are viral respiratory diseases, malnutrition , exposure to
cold, noxious gases, alcohol, drugs, and cardiac failure.
S. Sudden onset of shaking chills, fever, "stabbing" chest pain,
high fever ( IOI-IO50F. > » productive cough with "rusty" sputLin, and
occasionally vomiting. A history of recent respiratory illness ca: often
be elicited.
0. The patient appears acutely 111 with narked tachypnea
{30-*40/ninute) , but no orthopnea. Respirations are gruiting, nares
flaring, and the patient often lies on the affected side in an attempt to
splint the chest. Signs of consolidation may be lacking during the first
few hours, but fine rales and suppressed breath sounds are soon beard over
the involved area. Frank consolidation, involving part of a lobe or
several lobes, is found later. A pleural friction rub is often heard in
the early stages- Leukocytosis of ED-35 thousand/cu. ran, is the rule.
Crate-stained spotun shows many R.B.C., W.B.C., and pneunococci .
A. Pneunococcal pneunonia. Differential diagnosis: Other
bacterial pneumonias.
p. F^icillin C is the drug of choice. Give 600,000 units q. 12
h. IM for HKJderate cases. Severe cases will require up to 10 million
' uiits/2^ hrs by IV infusion. An adec|uate airway must be maintained, if
necessary, by tracheal suction, endotracheal tube, or tracheostomy. O2
must be supplied to any patient with severe pneunonia, cyanosis, or narked
dyspnea. Theat shock p.r.n. as outlined in chapter 15- Toxic delirluB
occirs in any severe pnetnonia and may be especially difficult to manage in
alcoholics. It is best controlled by pronazine 50-100 mg, IM q. *1. p.r.n.
Anxiety and restlessness nay be treated with phenobarbital 51-30 ng. q. flh.
Qie-taith gran phenobarbital h.s. helps insure adequate rest. Force Huid
to maintain a daily urina-y output of at least 1,500 cc. Liquid diet
intially then normal diet wh^ patient can tolerate it. £TH with codeine,
1 tsp q, 3-^- P-i*<n. Mild pleuritic pain may be controlled by spraying
the area of greatest pain with ethylchlor ide x 1 min, then along the long
axis of the body throi^ the entire area of pain, so that a line of frost
about 1 inch wide is formed. Codeine 15-30 mg. or taeperldine 50-100 7i>g.
may be used for severe pain .
(2) Klebsiella pneunonia. Occurs primarily in person 40-60
years of age with a history of alcoholism or debilitating diseases. The
causative organist is Klebsiella pneurtoniae, which occurs as normal
bacterial flora in the respiratory tract or gut.
S. Sudden onset of chills, fever d^pnea, cyanosis, and profoind
toxicity. The sputux is often red {“currant jelly"), nucoid, sticky, and
difficult to expectorate.
O. f^ysical findings and V.B.C. are variable. Diagnosis Is
based on finding short, encapsulated gram-negative bacteria as the
predoalnate organism in sputizD smears.
A. Klebsiella pneunonia. Differential diagnosis: F^eusococcal
pneinonia (you must have a good, well stained smear).
P. Kanamycin 0.5 gm IH q. 6-8h. (15 mg. /kg. /day) ; cephalothin
6-10 ^ IV. Antibiotic thierapy must be continued for at least three weeks.
General supportive care is the sane as for pneiii)ococcar~^euBon i'a'.
(3) Staphylococcal pneunonia. Pneunonia caused by
Staphylococcus aureus ocscurs as a sequel to viral infections of the
respiratory (ract (e.g.. Influenza) and in debilitated (e.g., postsurgical)
patients or hospitalized Infants, especially after antimicrobial drug
acteiinistration .
S. There is often a history of a mild illness with headache,
<»U^, and generalized aches that abruptly changes to a very severe illness
with high fever, chills, and exaggerated cough with purulent or
blood-streaked sputijn and deep cyariosis.
0. There nay be early signs of pleural effusion, empyema, or
tension pneunothorax tf.B. C. usually 20,000 cu. rm. Cram-staied sputui
reveals masses of W.&.C.'^s and gram-positive cocci, many of which are
intracellular.
A. Staphylococcal pnemonla.
1-21
1-22
P. Initial therapy (based on sputun smear) cOTsists of full
systemic doses of a cephalosporin, a penicillinase-resistant penicillin, or
vancomycin. The doses are as follows; cephalotin, 6-14 (jo/day IV;
■ethicLllin, 8-16 goB/day IV; varcomycln, 2 gm/day IV; nafcillin, 6-12
gn/day IV. If empyema develops, drainage must be established. If
pneunothorax develops, treat as described in chapter 16, Einergency War
Surgery.
(4) Streptococcal pieusonla. Usially occurs as a sequel to
viral infection of the respiratory bract, especially influenza or measles
or in persons with underlying pulBumary disease.
S. The patients are usually severely toxic and cyanotic.
O. Pleural effusion develops frequently and early and progresses
to efl^>yema in oTiC-third of untreated patients. Diagnosis rests in finding
large ntnber of streptococci in Ciraia-stained sputixn smears.
A. Streptococcal pneunonia.
P. Treat same as penunococcal pneLntonia.
b. Viral rneuKHiia.
S. Relatively slow progressive symptcms. Cough may be hacking
and dry or produce snail amounts of nonpurulent mucoid or watery sputm.
Rarely dyspneic. Usually associated signs of viral syndrome (e.g.,
myalgias, sore throat, ra^s, runny nose, conjuctivltis , etc.). Pleuritic
pain nay be present but is usLBally much less severe than in bacterial
pneixionia (splinting is rare)*
O. Usually only mildly febrile if at all. Does not appear
■toxic” as a rule- No chest findings of consolidation. Coarse breath
soinds and sometimes sparse rales may be heard. W.B.C. is usually normal
but may reach 12,000 or above with slight left shift (early) or right shift
(late in coirse). Cram-stained sputum: No organisns or few mixed
organisms.
A. Viral.
P. Iherapy: Symptomatic treatment.
c. Mycoplasmal pneunonia.
S. Resembles viral pnetmonia In symptomology but with slightly
more acute onset and more severe expression of symptcms. Cough is usually
more productive but sputun is similar in character. Malaise and myalgias
may be more proninent. Hay occur in limited, small group epidemics (camps,
schools, etc . ) .
0. Patient nay appear mildly toxic, fever may be high but is
usually low grade. Signs of consolidation in the chest. Leukocytosis (up
to 15,000) seen in only 25 percent of cases. Sir.uturr acfpears similar to
viral sputun.
A. Hycoplasna. Differential diagnosis; Chlamydia and
rickebtsia.
P- Therapy: Tetracycline P.O. 500 mg. q.4h. or erythromycin 500
Big. +to. Treatment is same for chlamydia and riokettsla.
1^. (MROHIC BRONCHITIS AND EMPHYSEMA.
a. Chronic bronchitis: A chronic airway disorder charactwized by
prodixstion of thickened secretions, recurrent bouts of infection, and
■icosal edema-bronchospaa]. Airway obstruction develops as the disease
worsens.
b. Emphysema: The term applied to distration and distortion of the
alveoli or terminal bronchioles.
S. (2wonic bronchitis is characterized by a cough that is
persistent or recurs daily for at least 3 months a year for at least 2
successive years. The typical cough is usually worse in the mcwning; the
patient continues to c»ugh until the urge is relieved by coughing up the
pool of mucous that has collected diming the night. A variable degree of
c^iest tightness and occasionally sane v^eezing may be noted in the tsorning,
but this too is relieved scmewhat once the chest has been "coughed clear."
As the disease becooes more advatxred, the cough worsens in severity and
duration, and sputum production increases. A significant smoking history
is almost always present. In the majority of cases it is a supperimposed
bout of respiratory infection that brings the patient to see you. JXiring
this time he usually notes a change in the color (green, brown or grey),
^hatTMt^ (thickened) or vofiBne (increased) ofsputum production. The
Migh may have become painful. Though a fever (usually low grade) nay be
present, significant degrees of dyspnea at rest are rare unless chronic
obstructive pulmonary disease (COPD) was present.
With the history of chronic cough and the morning distress, the
patient may also note a decrease in exercise tolerance secondary to
Shortness of breath. The greater the exercise intolerance the more
advanced the disease.
Suphysema: In the majority of cases, it will be associated with
chronic bronchitis, its signs and symptoms. The rare case of pir-e
onphysena usually presents with dyspnea on exertion. Cough Is usually not
proninent until COPD develops and, when present, is productive of only
anall amounts of watery mucoid Sputun. Likewise, repeated respiratory
infections are uncaonon .
Evidence of right-sided heart failure is inportant. In emphysema
its appearance represents the onset of the terminal ptese whereas in
chronic bronchitics right-sided heart failure may be tolerated for some
time.
0. In the early stages the findings on physical exan are
hCHispecific . Indeed, many exans will reveal no abnormalities to explain
the respiratory abnormalities.
Chronic Bronchitis: Scattered airway coarseness (rhonchi)
with cough is the most consistent finding. Occasionally, wheezes
^y be hea-d, but they are very mild and also clear somewhat with cough.
As the di^ase progresses in severity, some hyperexpansion of the chest and
prolongation of the expiratory phase may be noted.
Emphysema: Airway coarseness usually not as proninent.
1-23
1-2A
Ctherwise the findings are similar.
Lab: The onl^ lab study of any potential benefit in the field
will be &*am-staijied sputun. T^iis should be done to support a diagnosis of
infection. Though pneunonla tends to occur more frequently in these
patients, the rnost. ccmiiion Infection in this group is bouts of acute
bronchitis. {&*arn’s stain usually shows nod. W.B.C, (15,000-30,000), many
epithelial cells, and mixed flora.
A. Differentiating chronic bronchitis from asthrna may prove
difficult but certain differences are helpful.
Chronic Bronchitis Asthna
Cough Dcttinant feature, occurs Occirs usually in
chronically. association with attacl<
(e.g. wheezing,
dyspnea, etc.} .
Wheezing Mild, most notable in A.H. Dominant feature.
or during Infection;
clears scmewhat with cough.
Cyspnea Usually on exertion. At rest.
subacute in onset. Usually acute in onset.
H( of smoking Almost always present. Rare.
As both disorders progress through the years, the clinical
pictures became less distinguishable. Both, however, terminate in a
chronic obstructive lung disease with right heart problems. The
differences at this point, however, are academic b^ause treabnenb and
long-term management will be the sane regardless of the courses.
P, Hanaganent of less advanced cases of chronic bronchitis and
ODphysaa should be carried out as outlined.
(1) Halt progression of the disease process.
(a) Stop smoking; by far, the single most important factor,
Cb) Avoid areas inhere noxious fimes or high cc»icenbrations
of particulate matter (e.g., smoke, dust, fibers, etc.) are jH’esent.
(c) Chest percussion and postiral drainage in the morning
ar»d as needed through the day. The patient should be encouraged to
maintain hydration f2-3 liters of water per day).
(2) Functional rehabilitation. Progressive exercise programs
increase tolerance. Sene patients respond to bronchodilators so this
therapy is probably worth a try. Amlnophylline 200-*JCO irg. t.i .d.-q.i .d.
or theophylline 100-300 mg. t.i.d.-q.i.d. nay be given. Terbutaline 2.5-5
mg. t.i.d.-q.i.d. may be administered with either aminophylline or
theophylline. Some inhalants (e.g., Isuprel) may also be of some benefit
especially then a<±nini stered prior to a chest percussion and drainage
session.
(3) Infection management.
(a) Influenza vaccine Siould be received yearly.
(b) Pnemriococcal vaccination should be received.
(c) Acute bronchiti'" .jputun grari stain -♦5 nonspecific
(i.e., mixed flora); anpicillin or tetracycline 500 mg. P.O. q.6h. x 10
days. SputLSTi shows predominate orgmism: Treat as indicated (see
p^euDohia) .
(flj Severe bronchitis or emphysema.
(a) Stable: The same general therapeutic progran as
outlined above is initiated but with more urgency. Exercise programs, as
such, should not be attempted; rather the patient should be encouraged to
do as ouch for himself as possible.
(b) "ft-eakdown" is marked by a sudden wors^iing in
respiratory status (i.e., increased dyspnea, fatigiie, etc.). To prevent
[^egression to respiratory failure, some of the Treasures must be executed
rapidly and simultaneously.
J. An IV should be started and IV aminophylline
aMininistered as described in the astlxoa section. Rate should not exceed
125 cjc.yniin.
2. Terbutaline 2.5-5 mg. may be given SQ.
3- Antibiotics should be given. Treat with anpicillin
or tetracycline as described .
t- Oxygen may be given CAREFULLY if available. Cniy
Low Flow oxygen should be adainistered (2 liters/min) . High oxygen
concentrations can cause sudden respiratory arrest in the patient.
5- Durit^ the therapy the patient must be encouraged
to cou^ and clear as much secretion as possible.
6. Right-sided heart failure that is secondary to the
ling disease will only respond to improvement in pulmonary status. Digoxin
will not help. Diuretics nay precipitate shock, hence, should be avoided
in the field.
Z* l^sver give narcotics or sedatives that might
decrease respiratory drive.
i-26. H3LMCNARY EMBOLISM
a. Rjlmonary embolism occurs vAien a thrombus (blood clot) or foreign
matter lodges in the puleionary vascular bed (the pulmonary arteries or
their bry-ches) .
b. Etiology. The niost cermon type of embolus is a blood clot formed
part of the systemic venous circulation (usually deep leg veins),
that breaks loose to travel to and subsequently lodge in the pulmonary
circulation. Fat globules and amiotic Quid may also e*4K)lize to the
Death is usually the result of shock.
S. Chief ccmplaint: Sudden onset of unexplained dyspnea is the
1-25
1-26
most ccmon conplaint. This nay or may not be associated with chest pain ;
usually pleuritic (i,e., sharp, localized, aggravated by deep inspiration
or coughing) but rnay resemble Jthat of MI, Itenoptysls nay be a feature and
is usually seen when pulfltonary infarction has resulted* Syncope nay
sometiines be the presenting syreptom. By far the most consistent of these
symptoms is dyspnea. This conplaint also has some prognostic value, as
severe prolonged dyspnea is usually associated with very large emboli and a
poor prognosis .
Present Hx: Since 80-90 perc^t of pulmonary emboli are blood
clots, the patient should be questioned about any predisposing conditions.
These conditions are usually marked by stasis of venous blood flow with
subsequent clot formation. Question carefully for symptoBS of deep vein
thrombophlebitis in the legs (by far the most common source of emboli).
3Ye-exiStir^ congestive heart failure; shock states (traunatic, cardiac,
and septic); prolonged irtmobilization, either general (i.e., paralysis, bed
cor»finen»ent, etc.) or of an extremity (i.e., paralysis, cast, traction);
and post-op states are all associated with sluggish venous blood flow. In
pregns^t women clots may form in the pelvic veins. Severe cellulitis or
gangrene of an extremity may cause clot formation in large veins if these
veins are involved in the process.
Past Hx: A tendency toward recurrence has been noted in many
cases of pulmonary enbolian. A past Hx of pulmonary aibollstc or
inexplained signs and symptoms suspicious of pulmonary embolian are
helpful .
Occupational Hx: A high incidence has been noted in civilian
occupations with long periods of iimobllization (e.g., cab A truck
drivers). It is likely that similar itiilitary occupations might carry with
then seme predisposition toward clot fomatlon and subsequent enbolizatlon.
0. Physical findings are inconsistent and often absent with
small emboli. Generally the larger the embolus, the greater the pulmonary
and heflKKJynauic oonsecpjences, hence the more prominent the P.E. findings.
The patient is usually very anxious and in moderate to serve respiratory
distress. may grimace on inspiration (secondary to pleuritic pain) and
have one or both hands placed over the area t^re pain is greatest as if
wDinded there. He nay be pale and clamy if obstruction is great enough to
produce some degree of shock.
Vital Signs: Temperature is often slightly to moderately
elevated ( 38 - 39 ®C.) but may be subnormal if shock is present. Tachycardia
is the most consistent P.E. finding of the syndrene and has the same
prognostic implications of dyspnea. Note also postural changes (see B.P.).
Respirations are usually rapid and often some^^t ^llow (secondary to
splinting because of pein). B. P. may be normal. The presence of
significant postural drop in systolic B.P. may Indicate a high degree of
obstruction with poor cardiac output, h low systolic B.P. nay be seen when
frank shock has developed. Jse of accessory muscles of respiration is
usually seen only when the anbolus has triggered diffuse severe
bronchospasm (rare). Jugular venous distention may be noted (see
cardiovascular below). Asytnnebrical expransion between the two sides of ths
thorax may be seen secondary to pain (i.e, "splinting"). In the lings a
patchy area of e>a change or bronchovesicular (tubular) breath sounds and
rales may be discovered if some Itng collapse (atelectasis) has occurred.
Uheezing nay be detected if the embolus has Jiggered brochospaan. A
pleural friction rub may be heard if pulmonary infarction has resulted.
Dullness, e>a change with decreased breath sound may be present if a
pleural effusion is present.
Cardiovascular . Kussinaul’s sign (failure of the jugular veins to
collapse on inspiration) nay be noted. With large emboli, signs of acute
* right ventricular failure (see cardiovascular section) may be seen. Search
for signs of venous insufficiency or throfrtjophLebitls in the lower
extremities (the chief source of emboli).
A. Even with the aid of X rays and Lab facilities, the diagnosis
of pulnoQoary enfcolization may be elusive; pulmonary embolism may mimic
mvocardial Infarction, pneunonia, asthma, spontaneous pneunothorax , cardiac
tinponade, or virtLBlly any acute or subacute cardiac or pulmonary event.
The TOst consistent finding (tachycardia) is nonspecific am the other
findings are so inconsistent as to make formulation of any type of reliable
syaptoB-sign complex impossible- The so-called "classic triad" of dyspnea,
pleuritic chest pain, and tachycardia is neither specific nor regular in
occirrence. Pulmonary eirtoolism must first be thought of before it can be
diagnosed and it should be considered in any patient that develops sudden,
ifiexplained respiratory distress in a suspect setting. In the field, the
diagnosis will be a fmetien of three factors: O) historical and
physical findings; (2) the setting in which the event occurred (e.g.,
thrombophlebitis, prolonged iimnobilization , etc.); and (3) the exclusion
of other possible reasons for the distress (e.g., sudden onset of dyspnea
and tachycardia in a 22-year-old trooper liio has had a fractured leg
inBobilized for 3 days is unlikely to be having a myocardial infarction) as
rapidly and practical as possible.
P. Therapy: In the field, once embolization is suspected, very
little short of general supportive measures (e.g., oxygen, ventilatory
assistance, etc.) can be done to remedy the effects of the embolus. Large
or extensive enbolizatlon producing more than 70-8D percent of the
pulmonary circulation (depending or previous respiratory status and overall
health) will usually kill regardless of Supportive measures. Soaller
embolization (the majority) will begin to resolve within the first few
days, though significant improveoent in the patient's state ncay be noted
within the first hours. Since even small emboli nay produce very preaninent
signs and synptcxns initially, it is impossible to preict the severity of
the obstruction in the first hours after embolization. Vigorous supportive
Beasures must be instituted to give the patient's body as nuoh time as
possible for resolution.
Heparin therapy is instituted to prevent further clot foneation.
It does m t "melt" the clot already lodged in the pulmonary circulation
(though does assist resolution sootewhat) . Heparin nay cause fatal
bleeding if the dosages given are too high or the patient has another
disease process or injury (e.g., active peptic ulcer, hemorrhagic or
inflaonatory pericarditis, internal injuries, etc.) freo v*iich
wcontrollatole bleeding may occur .
Given Heparin: An Initial bolus of 15, OCX) to 20,000 units IV
followed by 7,500 imits SQ q.6h. or 10,000 units SO q.8h. Heparin therapy
must be taonltored; in the field, clotting time is the only practical
method.
1-27
1-26
Clotting Time: A stopvratch Is started when 5 cc. of venou:* blood
is drawn into a glass syringe. One ml. of blood is placed in each of three
dry glass test tubes. After 3 minutes the tubes are tilted every 30 sec
until the tubes can be inverted urithout blood spilling out. The elapsed
tines are noted in the 3 tubes and averaged to give the clotting ^ime {CT).
The test must be dene as close to 37 ^ C. as possible. This may be
acccmplished by taping the tubes to the abdonen of a volunteer. Have him
sit erect on the ground with outstretched legs and recline, gradually, back
on his elbows every 30 sec to check blood movement in the tubes. In warm
weather the tubes may be hand warmed. Itormal CT is between minutes,
but your monitoring should be based on a baseline measurement (e.g., a CT
done ^ior to heparin Rx). Subsequent levels should be drawn just prior to
administration of each intermittent dose. The goal should be to Taaintain a
CT of approximately twice the baseline measuretnent . fie par in” doses should
be rals^ or lowered accordingly. If on ^given dose t>» CT seems to
stabilize where you want it (for three consecutive readings) t you need only
obtain this measurement once or twice dally.
Heparin therapy should be continued until the patient's
cardiopulmonary status has improved. Once this occurs, the heparin luay be
tapered over ^<8 hours tx» 5j000 units 30 every 12 hours.
Progressive anbulation , before tapering the heparin, should be
encouraged. Ace wraps should be employed on the legs during this tiiDe.
The patient should be maintained cm 5,000 units SO every 12 hours
for weeks. This dose (often referred to as "mini-dose" heparin) will
not affect clotting times, so none need be done. This low dose does,
however, afford seme resistance to future possible clot formation.
Fat embolization: Should be suspected if sudden unexplained
dyspnea, tachypnea, tachycardia, and neurological deterioration {e.g.,
delirium, cena, etc.) develop 12-36 hours after bone fracture {especially a
major long bone or pelvic fracture). Treatment is supportive.
1-27- PLEURAL EFFUSIONS. The presence of fluid (including blood and puis)
in the pleural cavity.
Pathology: The presence of fluid displaces and restricts the lung on
the involved side, hindering respiration. The more fluid, the more
restriction. Fluid can arise fre® several processes {see below).
S. and 0. Progressive or worsening dyspnea is the most
consistent finding. The rapidity of fluid accunulation as well as the
amount of fluid present will contribute to the prominence of this sympton.
Slowly developing effusions may not produce significant -dyspnea until large
volumes have accimulated where a rapidly developing effusion will produce
dyspnea at smaller volumes. Other symptoms of pleural effusion will be
related to the specific causes. Deviation of the trachea away frea the
affected side may be seen. Poor movement of the involved side of the cLcst
may be noted. Dullness to percussion will be noted in the upright
position. The extent of dullness (measured to the intercostal space where
dullness disappears) should be marked off. Sometimes an area of
hyperresonanee will be noted just above the fluid level. Freaitu? is
absent. Decreased to absent breath sound is t)>e rule, but Lour:* tubular
breath sounds may often be present. Also whispered souna_ --ay bt absent or
less conmonly increase .
Lab: Pleural fluid should be examined and the following tests performed:
(1) W.B.C. count and differential; R.B.C. count.
(2) Gran's stain.
(3) Glucose measuiremfnt {dextrostix) of fluid and blood.
Other findings related to the specific causes of the effusion may be
present.
Congestive heart failure Usually right-side; ney be bilateral. W.B.C.
<1,000/WTi. 3/glucose equals serim glucose
R. 8 .C. <10,(X)0/inti. 3. Other evidence of
Cirrhosis As above but with evld«ice of liver disease.
Bacterial or viral Same side as infection. Hay precede other
pneiiDOTiia evidence of pneumonia. H.B.C.>1000p''nfn.3 with
>50%P.H.N.s/glucose<seriin glucose organisms
(bacteria) may be seen on Gran's stain (rare).
Tuberculosis Same side as infection. Other evidence of FTB
W.B.C. >l,0C»/nin.3 with >505 lymphocytes.
Pulmonary infarction Hay be bloody. R.B.C,>10,000 /bih.3
W.B.C.>1,000/Bm.5
Subphrenic ^scess W.B.C.>1,CO0/nn.3 (usually) evidence of intra-
abdcminal infection.
Chest trauma Frequently blood- Hx of trauma usually
obtainable.
Leakage Uvouigh a Fluid has characteristic of IV fluid used
subclavian line gluco 9 e>seruQ glucose (if D 5 was component
of fluids).
Pneuiothorax Usually unrenarkable but may have W.B.C.
increase .
P. Thoracentesis: Because of the danger of inducing a
pneuBothorax , evacuation of the fluid (therapeutic thoracentesis) should be
reserved for conditions iidiere severe respiratory distress is present. A
small Sampling of fluid may be obtained for studies (diagnostic
thoracentesis) relatively safely.
The major therapeutic effort should be directed at resolving the
process responsible for the effusion, [tost effusion will resorb once this
is done.
1-28. ASTltlA. A disease of the airways characterized by recurrent bouts
of dyspnea usually associated with wheezing and coughit^.
S. Chief complaint: Dyspnea is the most outstanding ccmplaint.
wset is usually abrupt (seconds to miTiutes) though there may occur, prior
to the onset of frank dyspnea, a period of vague chest discomfort not
^ways clearly defined upon questioning the patient, but often described as
a "rightness" by some. Hany asttwatics have learned to recognize this
aura" as a warning of impending attack. The dyspnea, when it does become
1-29
i-30
recognized, is usually progressive. Beeaiise the sensation of shortness of
breath is subject to modification by factors not directly the result of the
pathophysiology (i.e.» anxiety, intoxication}, ttie degree of apparent
dyspnea does not correlate well with the severity of airway obstruction;
hence it should not be used as a concrete clinical guide to therapy or the
patient's response to therapy. Cough is usually present and may be
productive of a thick, tenacious, grey-tihite sputun. This sputun riosbly
cor^sists of bronchial secretions that have "dried out" sooewhat (i.e., the
water is evaporated off by air flow leaving behind the thick aiucous
component of the secretions) ^d can reach the corsisteoey of gelatin.
This inspissated imjcous can plug airways, thus increasing airway
obstruction. Hence a dry cough in an asthmatic diring an attack may
indicate a severe degree of obstruction due to the "mucous plugging"
chencmena. Wlieezing may or may not be perceptible to the patient and is
defined further below. The duration between onset of syroptcms and
presentation should be obtained as the rapidity with which a patient
approaches a given anount of distress Cas obtained from history and
physical) nay prove a valuable index to the severity of the episode.
Past history: Host asthmatics are very familiar with their state
and tnay tell you both what usually triggers an attack and what therapy they
[.dually respond to.
Medications: Many attacks probably result from loss of medical
control. Determine wliat medications, if any, the patient uses for asthma.
If he discontinued them, determine when generally; the more medications and
the higher the dosages, the more severe his disease. Steroids are the "big
guis" of asthma therapy and the asthmatic requiring them for control has
sev^e disease.
Allergies: Some astimatics give a history of various and sundry
allergic responses (hives, rhinitis, etc.) to specific substances. These
patients are especially prone to anaphylactic reactions, so special
attention should be given to this segment of questioning. Mote here that
certain drugs can precipitate or worsen an asthma attack. The most notable
being salycilates and other nonsteroidol anti-inflaniaatory agents (e.g.
Indocin, Motrin, etc.) as well as propranolol (liideral).
0. General appearance. Asthcnatics appear anxious during an
attack, and the expression of fear on their faces is evident across a room.
Ihey inhale through open mouths often throwing their heads back as they do.
Exhalation nay be through pursed lips and the patient may le^ forward as
if straining to defecate. Astnaatics in moderate to severe distress prefer
to sit as maximal mechanical advantage of the respiratory muscles are
obtained in this position. When an asthnetic in this type of distress
"lays down" on you, it may indicate he is tiring; hence, you must move
quicKl y .
Vital signs: Should be obtained prior to any therapy.
Temperature, if elevated, may indicate presence cf a concomitant
infection .
Pulse is usually rapid and regular; slower irregular pulse may
indicate severe hypoxia acidosis. Pulsus paradoxus should be searched for
(see fi.P.) .
the resp'ir'ations should be noted- Because inspiration has more muscular
assist than expiration, air can be forced through partially obstructed
airways, but has considerably more difficulty getting out. Hjis results in
a prolonged expiratory phase, the length of idiich parallels roughly the
degree of obstruction. Further, as the patient breaths i aster (because of
hypoxia) his inspirations begin before the slower expirations are
cotipleted, hence air is trapped and the chest becocnes progressively
hypereipanded . As hyperexpansion increases, the amount of air the patiwit
is able to forcefully inspire decreases. He cempensates by breathing still
faster. More air is trapped and a vicious cycle ensues. For these reasons
a low respiratory rate with markedly prolonged expiratory ;^ase
(exhaustion) or a rapid shallow rate in the presence of marked
hyperinflation are pretenoinal events in the asthfnatic, . .seconds colkI.
B.P.: When the B.P. is markedly elevated (>160/>100) caution
should be used in the administration of epinephrine. The drugs should
probably be withheld altogether in the older patient with elevated B.P.
especially if there is a history of heart disease or stroke. The severity
of the elevation and the patient's overall state must be weighed together.
There are no hard and fast rules. An abnormal degree of pulsus paradoxus
(PP> should be searched for. When the cuff is inflated, SLCWLY deflate it
(Itm. Hg every 2 secs) and note at what point the systolic tones begin. If
pulsus paradoxus is present, these tones will disappear during inspiration
and reappear on expiration. Continue to deflate the cuff slowly and note
the range over >^iich this finding persists. If the finding persists over a
range greater than 12mj./rlg, there is an abnormal degree of paradox
present. This sign correlates well with the degree of obstruction (the
greater the range, the more severe the obstruction) and usually reflects
trends in the patient's status before they can be fully appreciated in
other aspects of the physical.
The degree of pulsus paradoxus should be noted through the
treatment ixitil normal and recorded with frequently collected vital signs.
In more severe degrees, the pulsus paradoxus may be noted in the peripheral
pulses where it manifests as an inspiratory disappearance or weakenit.g. of
t)ie pulse. This finding is an invaluable aid to estimating the severity of
obstruction and the adequacy (or inadequacy) of therapy when arterial blood
gases and other labs are not available or not practicable. A note of
caution here: A decrease in PP may be noted as the patiejit begins to
sucemb to exhaijstion or approaches the state of naxiTnal hyperinfiation.
Like any other physical sign, PP must be interpreted In light of the
gen-'ral clinical picture; yet here, any change is of significance.
HEENT - Dry mucous menA)ranes should be interpreted (as an
indication of possible dehydration) with caution as there is invariaciy
sane drying secondary to the praninent mouth breathing.
Beck - Use of the accessory muscles of respiration, specifically
the anterior and anterolateral neck muscles, have been shown to correlate
roughly with the degree of obstruction- Straining of these muscles
inspiration is seen in moderate to severe degrees of obstruction and their
use will decrease and eventually disappear as obstruction is relieved.
Remember , however, that use of these muscles will also become less
proninent as the patient becomes exhausted .. .ruonitor the WHCLE patient!
Chest - In the field, probably the most valuable indications of
the adequacy of ventilation are the magnitude and nature of chest
novooents.
Respirations are very important, fcth the rate at:d character of
1-31
L-32
For all practicable purposes if there is no chest exjiansion, the patient is
not iDovlng air. All the other paratneters used to monitor the asthniatic in
the field Ce.g., changes in PP; presence or absence of wheezes; use of
accessory muscles, etc.) should be interpreted in light of chest expansion
(and to a lesser extent on the presence or absence of breath sounds).
By the mechanism previously outlined , the chest may beccfoe
"locked In" a progressively increasing state of expansicnn by air trapping
and be unable to relax to its preinspiratory position. Since the chest
wall can only expand so far, the amo^^^t of air that can be forced in
progressively decreases. Signs of hyperexpansion include increased or
increasing anterior-posterior chest diameter {best noted at the end of
expiration); decreasir^ respiratory excursions; increasing chest
hyperresonaice to percLCSion with loss of cardiac area dullness and widened
intercostal spaces. In severe instances (approaching maximal
hyperinflation) air roovaneffit decreases to the point that breath sounds and
wheezes begin to fade and disappear. Expiratory movement: As stated
previously, the degree of expiratory pha.se prolongation should be noted.
Lungs - Breath sounds Bwy be heard in mild to rroderate states,
bub usutally beccne obscured by wheezing in more severe cases. Viheezlng is
a hallnark of partial airways obstruction. The sound is produced by air
"tiiistllng" through partially obstructed channels. Both inspiratory and
expiratory k*ieezes are heard in asthma though expiratory wheezes are more
prorainent and may be the only type present in mild episodes- As
obstruction is relieved, iiflieezing will diminish and clear breath sounds
in/ith improved respiratory excirsions will be nobed. Since the production
Of wheezes depends also on air flow, they will also diminish or vanish whwi
ventilation falls (e.g., high degrees of hyperexpansion or patient
exhaustion) . Here no breath sounds will be hei"d , and chest expansion will
be minimal to nonexistent.
Egophony C'e>a’ changes) may be noted in patchy areas over all
lung fields. In this case, the finding is probably secondary to collapse
of small areas of ling because their airways have been completely
obstructed- If the findir^ is very prominent over a fairly large, well
demarcated area, thsi an associated pnewonia or collapse of a ling
s^ent, lobe, or entire ling (depending on extent of the area) secondary
to obstruction of a bronchus by a large mucous plug must be considered.
Lab: An elevated W.B.C. count and/or leftward shift in the
differentiation may indicate an associated Infection. If this test is to
be pcrfomed, it should be <tone before a<*ninlstration of epinephrine as
this agent will itself increase U.fi.C. count in the leftwrd direction.
This effect may persist for 24 hours. Exam of the sputum may reveal tiny
mucous plugs that have been dislodged from the analier airways (called
Curschnann's spirals). Eosinophils may also be present in large nunbers.
The presence of m^y non-eosinophilic polisnorphonuclear cells should raise
suspicion of a possible associated pneimonia or bronchitis- In general,
however, most of the above provide merely supportive evidence, and since
more sophisticated labs will not be available, the diagnosis and rrvsnagement
of the asthmatic In the field will depend on your abilities to obta^ and
interpret clinical findings.
A. Asthma-
P. Hanagement: Therapy Is aimed at reversing the
pathophysiologic factors ihile correcting the derangements (e.g., hypoxia.
dehydration, etc.) they have produced. The treatment is staged to
correspond to the classes of severity previously outlined.
Mild Severe
.3-.5CC. 1;100 Administer epine phr ine
solution of as scheduled but irmediately
^inephrine SQ after first injection
re^^ q.^JOrnin x 3 or administer aminophylline as
until wheezes cleared follows:
Aminophylline 400 mg. in
250 cc. J )5 NS run
in IV over 15 tnin. Followed
by an IV atininistered
solution of aminophylline
200 mg. in 500 cc. 05 /V2
NS at rate of T50-2C0 cc./hr
until cleared.
If no improvement noted at 2
hrs or jMtient worsens,
continue infusion and,
Give terbutaline 0.25-0.5
mg. SQ. If no improvement
in 1 hr or patient wcH'sens
continue infusion and...
Give Solu-Medrol
(methyl prednisolone)
1 gm IV push followed by 1
grti IV push q. 6 h. until
clear. Solu-Cortef
(hydrocortisone)
may be substituted. An
initial TO ffn is given IV
push and subsequently q.fh.
thereafter intil clear.
Dehydration: p.O. hydration (force Hydration is accomplished
fluids) is usually with the arainophylllne
adequate solution. D 5 /l^? is
preferred but MS or Rir^er's
solution will suffice. CD 5 W
in extreme emergency).
Mypoxia: O 2 not required 02 - all attainable,
must be employed preferably
by mask (because of mouth
breathing)
secretions: Are thinned by hydration and released by relief of
to be effectively coughed up and cleared .
toieral therapeutic considerations: ffany would view this outlined plan of
?*®*^*' ” ^gressive. Ttowever, in the field, removed frcn
ao^micated di^nostic-monltoring facilities, mechanical ventilatory
1 ance, and most probably oxygen, the only hope the astlnatic has is an
1-33
If no improvement
noted or patient
wDrsens during Tx
E^onchospaan:
{-34
Section IV - Tne Circulatory System,
approach that relieves his obstruction ASAPJ The old adage of "push it
(sminophylline) till they puke" may be quite necessary in field practice to
assure adequate blood levels. It must be ren>embered that it is impossible
to reliably predict which episodes will respond to lower dos,^es or less
vigorous irianagenjent and that as the attack progresses your chances of
retrieval diminish by large factors. In these instances, you can expect
mortality rates approaching ?0 times those of a hospital emergency room.
Special Considerations:
Exhaustion: Close monitoring is necessary to head off complete
respiratory collapse. If the patient shows signs of "giving it up" (i.e.,
weakened respiratory effort raani Tested by a decreased or erratic
respiratory rate or decreased inspiratory excursicais associated with a
progressive decrease in breath sounds— or wheezes in the absence of breath
sounds— and a lethargic fatigued overall appea-ance) , therapy should be
stepped up by progressing directly to steroid administration. Talk to the
patient ar>d encourage him to hang in there? Slap him or pinch him if you
have to but try to buy any additional time you can. If he does not answer
coherently and continues to ''slip away," you must intubate and bag hita
ititil therapy begins to take effect and be can breath on his own.
Cyanosis: Slight discoloration may be noted at the nail beds and
sr>ould be managed by oxygen and continued broncbodilation therapy, khen it
occurs in the setting of impending exhaustion (above), it is an indication
for ironediate intubation and ventilatory assistance.
Hyperinflatiori; High degrees of hyperinflation associated with
decreasing excursions are an indication to step up therapy as outlined
ahwe. ^'Vice the chest becomes "fixed" at a high level of expansion,
however, ventilatory assistance can usually force no more air in than the
patient could. It should nonetheless be attempted since seme degree of
exriaustion is usually active.
l^rge mucous plugs; ^lay be relieved with hydration,
bronchodilators , and chest percussion. To perform percussion, the patient
is placed in a mshner to position the affected side up and in a head-doi/:i
tilt of approximately 305^ The area is briskly slapped with cupped palms
and the patient is asked to increase expiratory effort, if possible, or
cough.
Intubation: Once intubated the patient ' s own effective
mechanisms for clearing secretions (cough) are renraved. Frequent
Suctioning is a must. Never leave a tube in place in an asL?rnalic unless
you are ventilating him.
Iranediate follow-up therapy:
dice the patient has cleared, he should be placed on theophylline
103-300 iDg . t.i.d.-q.i.d. depending on severity of the episode.
Terbutaline rag. P.O. t.i.d ,-q.i.d. may also be given with this.
Those patieit-s that require steroid therapy should be placed on prednisone
NO mg. P.O. the first day after the episode and the dose reduced by b mg.
each day thereafter (e.g., 3^ mg. the 2nd day; 30 mg. the 3rd, etc.) until
they have been tapered to 5-10 mg. day. These patients and indeed ail
'severe cases should be evacuated as soon as possible for further
evaluation.
1 - 29 - circulatory system is composed of the heart, blood vessels,
Ijophactic system and their contained fluids, blood, and lymph.
a. Arterial hypertension. Elevation of systolic atKl/or diastolic
blexxi pressure, either primary (essential hypertension) or secondary.
Although the etiology of essential hypertension is unknown, the family
history is usually suggestive of hypertension (stroke, sudden death, heart
failure). Secondary hypertension is associated with kidney disease (e.g.,
chronic glomerulonephritis or pyelonephritis), or occlusion of one or trvore
of the renal arteries or their branches (renovascular hypertension). An
tntreated hypertensive patient is at great risk of developing fatal heart
faili.^e. brain hemorrhage, or kidney failure.
S. Prira»-y hypertension is asymptomatic until complications
arise. Ccmplications include left ventricular failure; atherosclerotic
heart disease; retinal hemorrhages , exudates, and vascular accidents;
cerebral vascular insufficiency; and renal failire. Hypertensive
encephalopathy due to cerebral vasospasm and edema is characteristic of
hypertension .
O. insistent diastolic pressure >liXi ran. ?ig in patients >60
years of age; diastolic pressure >90 ran. Hg in patients <50 years of age;
or systolic pressure >1h0 nm. Hg regardless of age. Retinal changes will
rar^e from minimal arteriolar narrowing and irregularity to frank
hemorrhages and papilledena , i.e., elevation of the optic disk or bli.yring
of the disk margins.
A. A Dx of hypertension is not warraited in a patient under 50
years of age unless the B.P. exceeds 143/gO ran. Hg on at least three
separate occasions after the patient has rested for 20 mirujtes or more in
quiet and familiar surrour.ding5. SecorKtary ccmplications will present
symptomatology of the '"target organs" involved:
(1) Cardiac involvement often leads to noctLmal dyspnea or
cardiac asthma (inspiratory and expiratory wheezing). Angina pectoris or
myocardial infarction may develop.
(2) Renal involvement may produce nocturia and hematuria.
The patient may have a urasic odor. Kidneys may be enlarged and palpable.
(3) Cerebral involvernent will demonstrate neurological signs
ranging from a positive Elabinksi or ibffman reflex to paralysis .
(4) Peripheral arterial disease causes intermittent
claudication (lunping). If the terminal aorta is involved, pain in the
buttocks and low back pain appear on walking and men beceme impotent.
P. Treat mild hypertension {diastolic pressure 92 to 113 irro. Eig)
with an oral diuretic such as chlorothiazide (Diuril) 500 ng. b.l.d. If
the dii^etic doe.s not control the hypertension, methyldcpa (AldcrTtet) 250
b.i.d. to 500 mg. q.i.d., or cionidine (Catepres) or reserpine 0.25 to
should be added. >tet>iyldop3 is preferred because its side
effects are better tolerated. For ooderate hypertersior (diastolic
pressure between lit ar.d 125 nrri. Hg) start tnerapy with an oral diuretic
and a sympathetic depressant (e.g., methyldcpa, clonlctlr.e, reserpine, or
propranolol) . For severe hypertension (diastolic pres?.:re >125 ran- Hg)
1-36
therapy should be started with an oral diuretic and guanekhidine (10 rng. to
150 mg. /day in a single dose) simultaneously. Methyldopa should be added
if needed. Patients with acute severe hypertension (diastolic pressure
>150 tm. Hg) or with pressures scrte^hat lower but with conwanding symptoms
of headache, visual disturbances, somnolence or other signs of cerebral,
cardiac, or renal involveioent or acute pulnjonary edema should be placed on
Strict bed rest ( seni-Fowler position) and parenteral therapy instituted
imiediately. Diazoxide (Hyperstat) is the drug of choice; 3CO mg. IV push
will reduce B.P, to normal values within 5 minutes. The drug should be
used only for short periods and ccmbined with a potent diuretic such as
furosemide (Lasix) 40 to 80 mg. IV. Vital signs must be monitored
continuously. Be prepared to treat hypotension (see Chapter 5, Shock).
Discontinue if any sign of hearing iopairment develops. When B.P. has been
brought under control, ccsibinations of oral sntihypertensive agents can be
added as parenteral drugs are tapered off over a period of 2-3 days.
b. Thrcni>ophlebitis. F^artial or ccnplete occlusion of a vein by a
throcBbus with a secondary inflarmatory reaction in the wall of a vein. It
occurs most frec^ently in the deep veins of the legs and pelvis in
postoperative and postpartun patients during the fourth to foij'teenth day,
and in patients with fractures or other traina, cardiac disease, or stroke,
especially if prolonged bed rest is involved. Deep venous thrombosis is
usually benign but occasionally terminates in lethal pulmonary embolism or
chronic venous insufficiency. Superficial phlebitis alone is usually
self-limiting without serious ccmplications; aging, malignancy, shock,
dehydration, anemia, obesity, and chronic infection are predisposing
factors.
S. Approximately half of patients with thrombophlebitis are
as^ptomatic : Others may ccmplain of a dull ache , tightness, or frank pain
in the calf or the whole leg, especially when walking. A feeling of
anxiety is not unccwnon .
clotting defect). Prior to initiation of heparin therapy, a baseline
clotting time must be established. (Normal Lee-White clotting time is 6-15
minutes). Ihe dose should be adjusted to provide 2-3 times the baseline
value. Continuous IV irifusion is the preferred route. Give a
as an IV bolus (2,000 units) prior to starting constant
infusion at a rate of approximately 1,500 units/hour for the average-sized
adult. Remember that the ultimate rate must be established on the basis of
clottinR times obtained from an arm not being infused and verified
by at least 2 successive clotting tines in the therapeutic range.
Subsequent clotting tines are repeated q.b-IOh. The required dosage will
usually decrease with time. If an infusion punp is not available, give
deep SO q.6h. (use small needle and inject slowly). Start dose in the
range of 7,000-9,000 units for an average-sized adult. Obtain clotting
time 30 minutes before each planned dose and adjust to maintain therapeutic
range. The required dose should drop to d, 000-6,000 units after a day or
two of therapy. Therapy should be continued intil the patient is
the danger of embolism has passed (normally 2-3 weeks).
The diagnosis of thrcnbcphlebitis is difficult without the use of
pretreatment
. loading dose
sophisticated diagnostic aids that normally are not available (phlebography
isotopic scan, etc.); therefore, naxieiun use must be made of past and
current history and the most thorough P.E. possible. The dangers of lethal
pulmonary anbolism must be carefully weighed against the dangers of
meontrolled heniorrhage , and each decision is made on a sound assessment of
all factors involved.
Prevention: The best cure for postoperative thrcnjbophlebitis is
its prevention. Assure that circulation is maintained by active and
passive exercise ^*ile patients are bedridden. Avoid tight clothing.
Elevate legs or foot of bed 15-30 degrees. Flex knees. Encourage deep
breathing exercise. AmbULLate patient as soon as possible (walking, not
standing). Dextran, 500 ml. IV during surgwy and repeated on first
postoperative day, appears to have a prophylactic effect, as does ASA 1 gm
daily P.O. NOTE : ASA is contraindicated once aiticoagulatlori therapy has
begin.
0. Slight swelling In the involved calf (measure); bluish
discoloration or prominence of the superficial veins; warmth of affected
leg when both legs are exposed to room temperature; tenderness and
induration or spasm in the calf muscles, with or without pain in the calf
produced by dorsiflexion of the foot (Hcnans' sign). With deep
thronibophlebitis involving the popliteal, ferooral, and iliac segments,
there may be tenderness and a hard cord nay be palpable over the Involved
vein in the fanoral triangle in the groin, Uie medial thigh, or popliteal
space; slight fever and tachycardia may be present. The skin may be
cyanotic if venous obstruction is severe, or pale and cool if a reflex
arterial spasm is superimposed.
c. HaDorrholds, Varicosities of the veins of the hemorrhoidal
plexus, often cooplicated by inflaniTiation , thrombosis, and bleeding. May
be external (distal to anorectal line) or internal (proximal to anorectal
line) .
S- Rectal* bleeding , pain (may be severe), itching, protrusion,
fAUCoid discharge from rectun.
fli. Small, rouhded, purplish skin-covered masses that are soft
^2? painful unless thrombosed. When thraobosed, they are hard and
often extremely painful when palpitated.
A. Thrombophlrtiitis . Differential diagnosis: Calf muscle
strain or contusion. NOTE: Pain due to muscular causes is absent or
minimal on dorsiflexion of the ankle with the knee flexed and oaxiioal on
dorsiflexion of the ankle with the knee extended or during SLRs (Homans'
sign); cellulitis; lymphatic obstruction; acute arterial occlusion (distal
pulses are absent and there is no swelling); bilateral leg edena due to
heart, kidney, or liver disease.
P. Treatment: Strict bed rest; elevate legs 15-20 d^rees. Ace
bandage from toes to just below the knees; moist heat. Anticoagulation
therapy with heparin should be initiated if there are no contraindications
to its use (contraindications are peptic ulcer, significant kidney or liver
disease; Hx of cerebrovascular hemorrhage, recent head traijna, or known
A. Hemorrhoids (Internal or external). Differential diagnosis:
renanal ^ess, rectal neoplaans, or colitis.
. P* stool softners or nonirrltating laxatives, such as
<iiet to prevent hard stools and straining. Small
banorrholds are usually self-limiting and respond well to
minimal treatment, fenage local pain and infection with
oaths and insertion of a soothing anal suppository b.i .d ,-t.i .d.
i.'^ )>®nzocaine and other types of similar olnbnents as much as
t i ri sensitizing the patient. Use hot sitz baths
* ■ --q.i.d. to reduce throobosed hemorrhoids. If this is unsuccessful or
1-37
1-38
patient is in extreme disconfort, excise the thromtKJS tjrvder Tt lidocaine
local: pack lightly with icdofomi gauze ihitially and cover with dry
sterile dressing. Change dressing daily- Continue warm sitz baths.
Instruct patient to avoid trauna u.hen cleansing the anal area after bowel
novements by patting with damp tissue rather than rubbing. Instruct
patient rot to attempt to defecate unless there is a real urge and to avoid
straining at stools.
1-30. DISEASES OF THE HEART.
a. Myocardial infarction {Ml). Ischemic myocardial necrosis usually
resulting frcn a sudden reduction in blood flow to a section of the
nyocardium due to occlusiwi of a coronary artery.
S. Sudden onset of intense, crushing substernal or precordial
pain, often radiating to the left shoulder, arm, or jaw. Patients break
out in a cold sweat, feel weak and apprehensive » and move about seekir^ a
position of comfort. They prefer not to lie quietly. Lightheadedness,
syncope, dyspnea, orthopnea, cough, i^eezing, nausea and vcmiting, or
abdcminal bloating nay also be present, singly or in combination. The pain
is not relieved by nitroglycerin .
0. Patient may be cyanotic and the skin is usually cool- The
pulse may be thready and the blood pressure variable, rtast show some
degree of hypertension inless cardiogenic shock is developing {inciderwe
about 8-14 percent). In a severe attack, the first and second heart sounds
are faint and often indistinguishable. Arrhythnia is ccmmon. Rales may be
heard on auscultation and the neck veins are often distended. Fever is
absent at the onset but usually rises to IOO-1030 p. within 24 hoirs-
U.fl.C. will be elevated with a shift to the left by the second day. The
sedimentation rate is normal at onset and will rise on the second or third
day.
A. Acute myocardial infarction. Differential diagnosis: Angina
pectoris, acute pericarditis, acute pulmonary emboliaa, reflux esoph^itis,
acute pancreatitis, acute cholecystitis, spontaneous pnetiwthorax ,
pneumonia.
P. Be alert for cardiac arrest, particularly during the first
few hours after onset <50 percent of all MI deaths occur during this
period)- Be prepared to initiate CPR immediately if patient does arrest
(see Chapter 3i uuergency Resuscitation). Morphine ^4 ^ .
stat. repeat q- 15 «in p.r.n. u nless respiration falls below 12/min . Shock
option O2 positive pressure) . Lidocaine initial bolus
^-100 tng. fl mg. /kg.) IV, then n drip at 1-4 mg. per minute. Hospitalize
with strict bed rest and complete nursing care for at least 6 weeks.
Sedate with sT^onobarbital t.i.d. Low sodiun, low fat, low protein
diet. Itjnitor vital signs constantly. Be alert for signs of left-sided
heart failure (see para e, Congestive heart failure), hypotension, and
cardiogenic shock (see Chapter 15, Shock); evacuate feasible.
b. Acute myoc arditis . A focal or diffuse Inflammation of the
myocardium occurring during or after many viral, rickettsial, spirochetal,
fingal, and parasitic diseases or administration of various drugs. Severe
myocarditis occurs most connionly in acute rbeinatic fever, diphtheria,
scrub typhus, and Chagas* disease.
S, Fever, malaise, arthralgias, chest pain, dyspnea, and
palpitations. The patient may have associated pericarditis, with chest
Min characteristic of pericardial involvement {see para f. Acute
^picarditis) . The chest pain is frequently vague and noridiagnostic .
0- Tachycardia out of proportion to the anount of fever. The
B.P. Is usually normal. AuscuLation may reveal a tic-tac rhythm and
systolic fflurmur. Acute circulatory collapse, errtboll, and sudden death aiay
occur -
A. Acute myocarditis. Differential diagnosis: Viral,
protozoa), or bacterial infections must be distinguished from acute toxic
m^arditis due to drugs or diphtheria and from myocarditis associated with
azute rheirtatic fever and acute glomerulonephritis by a careful analysis of
each history and clinical picture as it presents.
P. Direct treatment toward underlying cause if knovn. In all
cases when myocarditis is suspected or apparent, complete bed rest and
sedation plus continued therapy of the underlying disease are needed.
Oxygen is indicated when cyanosis or dyspnea occurs. Continue bed rest
until all evidence of cardiac involvement disappears.
c. Bacterial endocarditis. Bacterial infection of the lining
■enbrane of the heart. Acute bacterial endocarditis (ABE) begins abruptly
and peeresses rapidly. The usual cause is staphylococci and occasionally
pneuMOCOCCl. It may follow postabortal pelvic lnfeclic«i, surgery on
infected tissue, or unsterile intravenous techniques. Subacute bacterial
endocarditis (SB£) is usually due to alpha-hanoliticus streptoc-occi and
frequently follow a dental procedure. The disease is fatal if untreated.
S. Fever is usually present but afebrile periods nay occur*
Might sweats, chills, malaise, fatigue, anorexia, weight loss; myalgia;
arthralgia, or redness and swelling of joints; sudden visual disturbances;
paralysis; pain in the abdomen, chest, or flanks; nose bleeds; easy
bruisability ; and symptans of heart failure may also occlt.
0. Findings in SBE include tachycardia; splenccnegaly; petechiae
of the skin, mitcous membranes, and ocular fundi, or beneath the nails as
splinter hemorrhages; clubbing of the fingers and toes; pallor or a
yellowish-broMi tint of the skin; neurologic residual effects of cerebral
tender finger and toe pads . In ABE symptoms and signs are
^ those of SBE, but the course is more rapid. Suspect AB£ if an
^Qlthy individual with a focal infection suddenly develops
fever, and prostration . An unexplained fever in patient with
ateart nurmur is indicative of endocarditis. Anemia, markedly elevated
i"ate, variable leukocytosis, microscopic hematuria,
proteiniria, and casts are commonly present in SBE and ABE.
Infective endocarditis due to .
^ diagnosis: Lymphomas, thrombocytopenic purpura, leukemia,
^'heLfnatic fever, lupus erythematosus, septicemia (may be the
forerunner), lprls.
dailv .^^^arditis due to streptococcus: Penicillin G 20-40 H.U.
Q 2-4h i gm daily in divided doses as bolus injections
infusion. Probenecid 0.5 ©n P.O. t.i.d. x 4-5 weeks.
>ns./^ kanaaycin 15 rag. /kg. /day; or gentamicin 5
-d.-t .i .d . in divided doses. Endocarditis due to
us (penicillin resistant), nafcillin, 8-12 gm daily as a bolus
1-39
1-40
q.?h. in an IV Infusion. If patient is hypersensitive to penicillin,
desensitize or use vanccnycin ?-3 SPi IV daily in divided doses q.Uh.
continue Tx x 5-6 weeks. Ccnplete nursing care. Monitor for signs of
neurotoxicity and thrcabophlebitis. Change injection site q.48h. and keep
Scrupjlously clean. Evacuate if at all feasible.
d. Angina pectoris. A clinical syndrome due to myocardial ischenia
producing a sensation of precordial disccmfort, pressure, or a strangling
sensation, characteristically precipitated by exertion and relieved by
rest or nitroglycerin.
S. Squeezing or pressurelike pain, retrosternal or slightly to
the left, that appears quickly during exertion and increases rapidly in
intensity until the patient is ccmpelled to stop and rest. The
distribution of the distress ciay vary widely in different patients, but is
always the same for each individual patient. The attacks usually last less
than 3 minutes unless following a heavy meal or precipitated by anger, in
which case they may last 15-20 minutes. The distress of angina is never a
sharply localized darting pain that can be pointed to with one finger. If
the patient points with one finger to the area of the apical impulse as the
only site of pain, angina may alnwst certainly be ruled out.
O. The di^nosis of angina pectoris depends alioost entirely upon
the history, and it is of utmost importance that the patient be allowed to
describe his symptoms to the examiner. The diagnosis is strongly supported
(1) if 0.^ Bg. nitroglycerin inv»-iably shortens an attack and (2) if that
anount taken irrmed iatei y before hand invariably permits greater exertion
before onset of an attack or prevents it entirely. Exanination during an
attack frequently reveals elevated B.P. ; occasionally, gallop rhylhu is
present during pain only.
A. Angina pectoris. Differential diagnosis: Musculosketal
disorders, cholecystitis, reflux esophagitis, peptic ulcer, myocardial
infarction.
P. Nitroglycerin 0-3 sublingually is the drug of choice-
increase dose to 0.4-0. 6 mg. if smaller dose is ineffective, Che anyl
nitrite ampule crushed and inhaled will act in about 10 seconds. The
patient should stand still or lie cioivn as soon as the pain begins and
remain quiet until the attack is over. Patients should be warned not to
try to work the attack off-
e. Congestive heart failure. A clinical syndrcrue in which the heart
fails to maintain an adequate output, resulting in diminished blood flow to
the tissues and in congestion in the pulmonary and/or systemic circulation.
The left or right ventricle alone may fail initially Casually the fonraer),
but ultimately ccmbined failure is the rule. The basic causes of
ventricular failure are: Cl) Myocardial weakness or inflaaretion (e.g.,
myocarditis, ischemia), <2) Excess workload (e.g., hypertension, aortic
insufficiency anemia, pregnancy, etc.).
5. Early manifestations of left ventricular failure include
undue tachycardia, fatigue with exertion, dsypnea with mild exercise, and
intolerance to cold; paroxysmal nocturnal dyspnea and cough. In advanced
failure severe cough is promlnentT” TTie ’sputum may be tinged rusty or
broun. Frank hemoptysis is rare but car occur. Ac ute pulmo n ary edema is a
serious life threatening manifestation of left ventriciUar failure. The
patient presents with extreme dyspnea, cyanosis, tachypnea, hyperpnea,
restlessness, and anxiety with a sense of suffocation. Right ventricular
failure presents with increasing fatigue, awareness of fullness in the neck
imH abdomen, anorexia, bloating, or exertional RUQ pain. Oliguria is
present in the day time; polyuria at night.
0. Signs of left ventricular failure include reduced carotid
pulsation, diffuse apical irspulse, palpable and audible third and fourth
he^t sounds, inspiratory rales, and pleural effusion. With acute
pulmcna'y edema the pulse may be thready and the B.P. difficult to obtain.
Respirations are gristing and l^jored with in^iration, and expiration is
prolonged. Expiratory rales can be heard over both lungs. Th^e may be
^ked bronchospaan or wheezing. Hypoxia is severe and cyanosis deep.
Patients with right ventricular failire show signs of venous hypertension,
ai enla'ged and tender liver, mamurs, and pitting edai^a of the lower
extremities. CBC and sed. rate are normal in unccMplicated left heart
failure. Urinalysis often shows significant probeinie-la and granular
casts.
A. Congestive heart failure due to . Differential
di^nosis: Pericardial effusion, c»nstrictive pericarditis, pulmonary
disease, carcinoma of the ling, anemias, and reboixid edema following the
use of diuretics.
P. Bed rest (Fowler* or semi-Fowler position), sedation with
morphine or (dienobarbltal ; frequent (4-6) aiall , bland, low calorie, Low
residue, sodium restricted meals with vitanin supplements. Diuretics such
as hydrochlorothiazide 50 ing./day or chlorothiazide 500 mg. daily or b.i.d.
are essential to management of chronic heart failure. Increase daily
ingestion of foods with a high potassiun content (bananas, orange juice)
for potassium replacauent. Ac^inister Oj p.r.n. for respiratory distress
and hypoxia. Acute pulmonary edema is grave medical emergency demanding
arwJ effective Tx^ Unless in shock, the patient should sit upright
with legs dangling. Give high concentrations of 02 ty mask or nasal
cannula. Ifcrphine SO 4 5 - 1 O mg. IV or IH. Sublingual nitroglycerin D.M-D.6
mg- q.10 min for several doses nay be imtediately effective. If severe,
apply B.P. cuffs (or soft rubber tourniquets) to three limbs and inflate or
tighten sufficiently to obstruct venous return (midway between systolic and
diastolic pressire) but not arterial flow. Rotate q,)5 rain. NOTE : Do not
apply to a limb in which an IV is runnir^. If IV is rurming, deflate
q. 15-20 min but do not rotate. Give a rapid acting diuretic, e.g., Lasix
(furosenide) 40-B0 ng. IV or Edecrin 25-50 b«. TV. Aminophylline, 0.25-0.5
slow IV or aminophylline suppositories, 0.25-0.5 gm may be of help.
Rapid digitalization is of value; however, it raust be remerabK-ed that all
digitalis preparations are toxic and the difference between the therapxitic
and toxic level is small. Do not use digitalis if there is indication
w renal failure. If renal function is normal , the following schedule may
used: Digoxin 0.25 mg. IV or P.O. stat., then 0.25 "g- q.6h. x 2 days
aw 0-25 mg. daily thereafter. NOTE : Digitalis mainten£«ce nay be
^uired for the remainder of the patient’s life. When stable, the patient
uld be carefully monitored for: (1) Status of original s^riptoras, (2)
(3) weight chaises, (4) vital signs, (5) evidence of
i*uebothrombosis. Evacuate as soon as feasible.
res pericarditis. Inflammation of the pericardiin. It may
u t froa trauna, infection, or neoplasm or secondary to systemic
iseases such as rhetmatic fever, rheijuatoid arthritis, or uremia.
S- Pleuritic or persisting substernal or precordial pain
1-41
1-^1 2
radiating to the neck, shoulder, or back. Pain nay be aggravated by
thoracic motion, cough, and respiration. It is relieved by sitting up and
leaning forward and may be accentuated by swallowing. Tachypnea,
nonproductive cough, fever, chills, weakness, and anxiety are cormon.
0. Auscultation reveals to and fro fhiction sounds {friction
rub) over 4th (L) intercostal space near stermin. inspection and palpation
sometinaes reveal a diffuse apex beat. With purulent effusion may present
vfith high, irregular fever, sweats, chills, and progressive pallor.
Bulging of the precordlum, increased dullness to percussion, and edasa of
the precordium may also be preset. Leukocytosis and elevated sed. rate
will be present at the onset .
A. Acute pericarditis due to . Differential
diagnosis: Acute HI, pleurisy.
P. (1) Treat inderlying condition.
(2) ASA 600 mg. P.O., codeine 15-60 mg. P.O. , meperidine
50-100 tag, P.O. or IM, or morphine 10-15 teg. SO q.4h. for pain. Sedate
with phenobarbiUl 15-30 n«. P.O. t .i .d.-q .i -d. ; 100-200 mg. phenobarbital
nay be given h.s. for insomnia- Prednisone 20 to 60 ng. daily in divided
doses t .i .d .-q.L .d. may be required to control pain, fever, and effusion.
The dose should be reduced gradually and discontinued over a period of 7-14
days. If the pericarditis is due a pyogenic infection, surgical drainage
of the pericardial sac may be indicated.
1-31- DISEASES OF THE BLOOD.
a. Anemia [general), A condition in t*iich there is a reduction in
the nunber of circulating R.B.C.s and/or Hb in the blood. Findanentally,
all anemias are caused by one of the following conditions:
<1) Increased loss of R.B.C. due tor
(a) Hemorrhage.
(b> Increased rate of R.B.C. destruction (hemolytic
anemias) .
(2) Decreased production of R.B.C. due tor
(a) DeficiefXiies.
(b) Bone marrow suppression .
b. Iron-deficiency anemia. Chronic anemia characterized by snail,
pale R.B.C, and depletion of iron stores. In adults it is almost always
due to occult blood loss (G.I. bleeding, excessive menstrual , excessive
salicylate intake, etc.).
5. Easy fatigability, dyspnea, palpitation, angina, and
tachycardia. In^ility to swallow or difficulty in swallowing may exist in
advanced cases. There often exists a craving for strange foodstuffs (dirt,
chalk, paint, etc.).
0. Skin and mucous membranes are usually pale. In advanced
cases the skin may have a waxy appearance; the hair and nails are brittle,
lor^ibudinal ridging with progressive concavity (spooning) may appear on
the fingernails. The tongue may be smooth, and the lips inflamed and
cracked. Hb may be as low as 3 Hgl
W.B.C. is noTwal.
but R.B.C. is rarely below 2.5 m.
A. Iron deficiency anemia due bo^ _. Differential
di^nosis* Other hypochrcmic anemias (anemias oTTnTection , thalassemia,
etc.) pernicious anemia, aplastic anemia.
p. (1) Treat umderlying cause.
(2) Oral FeSOij 0.2 gm t.i.d. p.c. Continue for T months
after Hb returns to normal. If there is bleeding in excess of 500 ml./iA
over a sustained period, iron therapy will not work until the cause of
bleeding is corrected. NOTE: Iron causes a color change in the stool
(dark green or black). Advise patient not to be alanoed if this occurs.
C, f^miciOUS anemia. Anecia due to impaired absorption of vitanin
B12*
S. Same as iron deficiency. In addition the patient may
ccoQilajii of a "burning of the tongue"; constant, symmetric mjchness of the
feet; various G.I. disturbances (anorexia, constipation, diarrhea, vague
abdotiinal pain); transient paresthesias of the URier extremities; aid
severe weight loss. There may be mental disturbances ranging from mild
depression to deliriLn and paranoia.
O. Pallor with a trace of jaixidioe; loss of vibratory sensation
in the lower extremities, loss of positional sense, loss of coordination ;
hyperactive deep tendon reflexes and positive Babinski. Occasional
splenomegaly and hepatomegaly may be present. Differential smear will
deoonstrate large oval R.B.C. with a few small misshapen R.B.C. W.B.C. is
usually less than 5,000. The granulocytes tend to be hypersegmented .
A. Pernicious anemia. Differential di^nosis; Anemia due to
folic acid deficiency. NOTE: The oval shape of the R.B.C. and
hypersegraentation of the W.B.C. are not characteristic of folic acid
deficiency anemia.
P. Give 100 tog. vitamin stat., then 100 rt^. 3 times per
week Lxitil blood pictire returns to normal. If anemia is severe, give
transfusion (after type and X-match) of packed red cells slowly.
d. Her»lytic transfusion reactions. Hemolysis of the recipient's or
*>hor's R.B.C. (usually the latter) during or following the administration
of solutions, plasma, blood, or blood ccraponerts. Hemolytic reactions vary
in severity depending on the degree of incompatibility, the amount of blood
arw the rate of administration. The most severe reaction occurs
Wien donor R.B.C. are hemolized instantaneously by antibody in the
recipient's plasma. These reactions constitute a grave medical emergency.
S. ^ Sudden onset of chills and fever and pain in the vein at the
site or in the back, chest, or abdomen. Anxiety,
^^ehensior, and headache are ccmnon. Under general anesthesia,
Pontaieous bleeding may be the only sign of a transfusion reaction.
nrvvrr..^- • Evidence of shock (see Chapter 15, Shock). Oliguria, anuria,
pr^ressing to urania. If a hanolytic reaction is suspected, imiediately
a bl^ sample froB the patient and centrifuge it. Hemolysis will be
early visible as a pink to dark red color in the serin.
1-43
4
1-46
A. Heiaolytic transfusion reaction. Differential diagnosis:
Hinor allergic reactions. (Serum will raoain clear.)
P. (1 > STOP TflAKSFUSIOK STAT.
(2) Treat for shock.
(3) To prevent renal failure, give 10% mannitol solution IV
infusion at a rate of 10-15 ml. /min until 1,(XX) ml. have been given. If
diuresis occurs, continue the mannitol infusion intil serum and urine are
clear .
1-32, DISEASES CF LYNfHATlC SYSTEM.
a. Lymphadenitis- Inflannatlon of one or more lymph nodes. Usually
secondary to a primary infection elsewhere involving the skin or
subcutaneous tissue.
S. &Llarged, tender, often acutely painful IjiViph nodes.
Systemic symptcns may be minimal or severe .
O. Primary focus of Infection in the region of the affected
node(s). Cellulitis, suppuration with abcess formation may occur. Low
grade or chronic infections may produce firm, nontender nodes that persist
indefinitely Ce.g., TB and fungal infections). They oay form cold abcesses
or erode through the surface to create draining sinuses.
A. Lymphadenitis secondary to Differential
diagnosis: Lymphedema secondary to blockage of the lymph channels.
P. Treat primary Infection. Apply moist beat to localize
infection. Aialgesics for pain. lAD abcesses.
b. Lymphangitis. Acute or chronic inflaaiTHtion of the superficial or
deep lymphatic channels, usually caused by streptococci or staphylococci.
S. Fever (102 to 1050 F-), chills, malaise, generalized aching,
and headache.
O. Patchy areas of inflamriation along the path of a lymphatic
channel resembling cellulitis. Lymphangitis occurring as the result of
hand or foot infection presents as irregular pink, tender, linear streaks
extwding toward the regional lymph nodes. Lymphadenitis usually follows.
Leukocytosis (W.B.C. 15,000-30,000) with shift to the left.
A. Acute lynpangitis due to . Lj.fferential
di^nosis: Acute thrc«pofKlebitis, cellulitis.
P. Treat the original Infection, but avoid all undue surgical
maiipulation of the woind. Use same antibiotic therapy as for acute
cellulitis (Chap 1, Sec I). Jkitibiotlcs should be continued tntii the
temperature has been normal for 72 hours and infletwiation has subsided.
Section V - Digestive System
1-33* GENERAL. The digestive system covers the entire alimentary tract
/^oyth, esof^gus, stomach, intestines, colon, and rectui) and all organs
that aid in digestion (liver, gallbladder, and pancreas). Diseases of the
mouth are covered in the dental section. Diseases of the esophagus are
either minor or of such a nature that we can only treat them
symptomatically.
1 . 34 . ACUTE ABDOMEN. Usually manifested by pain, anorexia, nausea,
vcnuting, and fever. Physical exan shows tenderness, muscle spasm, and
changes in peristalsis. Correct diagnosis depends on the precision and
care in taking history and doing physical exans.
a. History-
(1) Node of onset of abdominal pain.
(a) Patient is well CHie moment and seized with agonizing
(explosive) pain the next; most probable diagnosis is free rupture of a
hollow viscus or vascular accident. Renal and biliary colic may be very
sudden in onset but are not likely to cause severe and prostrating pain.
(b) If pain is rapid in onset — moderately severe at first
aid becoming rapidly worse — consider acute pancreatitis, mesenteric
throitesis, or strangulation of the small bowel.
(c) Gradual onset of slowly progressive pain is
characteristic of peritoneal infection or inflarisation . Appendicitis and
diverticulitis often start this way.
(2) Character of the pain .
(a) Excruciating pain not relieved by narcotics indicates a
vascular lesion such as massive infarction of the intestine or rupture of
an abdcriinal aneirysm.
(b) Very severe pain readily controlled by medication more
typical of acute pancreatitis or the peritonitis associated with a ruptured
viscus. Cbstructive appendicitis and incarcerated small bowel without
extensive infarction occasionally produce the sane type of pain. Biliary
or renal colic is usually promptly alleviated by medication.
(c) Dull, vague, and poorly localized pain usually gradual
in onset strongly suggests an inflammatory process or low grade Infection,
®-g., appendicitis.
(d) No abdominal pain but complains of feeling of fullness
might be relieved by a bowel movement, enema provides no relief (’'gas
®*^ppage sign"). This may be present when any inflammatory lesion is
walled off from free peritoneal cavity.
. (e) Intermittent pain with craiips and rushes ccnmoniy seen
i^^stroenteritis. The peristaltic rushes have little or no relation to
aManinal cratips in gastroenteritis. If the pain comes in regular cycles,
^sing in crescendo fashion, synchronous with the pain and then subsiding
a pain-free int«-val, small bowel obstruction is very likely.
1-46
(f) Radiation or a shift in localization of pain. Pain in
the shoulder follows diaphragmatic irritation due to air, peritoneal fluid,
or blood. Biliary pain is o^en referred to the right scapula and rarely
to the left epigastrium and ’left shoulder, simulating angina pectoris.
Classically, appetxlicitis begins in the epigastriun and settles in the
right lower quadrant. A shift or spread of abdominal pain often indicates
:^reading peritonitis.
<g) Anorexia, nausea, and vcniting. The time of onset of
these symptoms is important; if they precede the onset of pain,
gastroenbwitis or some systemic illness is much more likely the di^nosis
than acute abdominal disorder requiring an eewrgency operation. The most
likely possibilities are gastroenteritis, acute gastritis, acute
pancreatitis, ccmwon duct stone, and high intestinal obstruction. Inmost
other acute sirgical emergencies, nausea and voniting are not dominant
symptoms though they may be present.
(h) Diarrhea, constipation, and obstipation. Some
alteration of bowel finction is cormon in most cases of acute abdominal
emergencies. Diarrhea is the classic manifestation of gastroenteritis, but
it may also be a dominant syraptoffi of pelvic appendicitis. Bloody and
repetitive diarrhea indicates ulceration of the colon, but you should
consider bacillary or amebic dysentery first.
(1) Chills and fever. Repeated bouts of chills and fever
are characteristic signs of pylephlebitis and bacteremia. Chills and fever
are comon in infections of the biliary or renal tract. Acute cholangitis
and pyelitis present with intermittent chills and fever. In appendicitis ,
fever is not usually very high and there are usually no chills unless you
have a perforation. In a woman with no apparent general systemic illness,
a very high fever with peritoneal signs is characteristic of acute pelvic
inflammatory disease (FID).
b. Routine for physical exan of the acute abdcmen.
(1) General inspection (patient standing).
{2) Cough tenderness. Examine hernial rings and male genitals.
<3) Feci for spasm.
<^) Ore-finger palpation.
(5) Costovertebral check for tenderness.
(6J Deep palpation.
(7) Rebound tenderness.
(3) Auscultation.
(9) Rectal and pelvic exanination.
!-35- DISEASES OF THE ST-OMACH.
a. Acute simple gastritis. This is probably the most common
disturbance of the stcmach and is frequently accompanied by generalized
enteritis. Causes are chemical irritants (e.g., alcohol, salicylates),
terial infection or toxins (e.g., staphylococcal food poisoning, sc
r ^ poetronia) , viral infections (e.g., viral gastroenteritis, meas
influenza), and allergy (e.g., shellfish).
, scarlet
measles,
S. Anorexia is always present and may be the only symptom.
Usually r patient complains of epigastric fullness and pressure ar>d nausea
arid vomiting. Diarrhea, colic, malaise, fever, chills, headache, and
■ttscle cranps are ccnmon with toxins or infections.
0. The patient may be prostrated and dehydrated. Ejtarniration
shows mild epigastric tenderness. Hemorrhage is frequent with chemical
irritaits te.g., salicylates). This may be found using a guaiac test. CBC
nay show a leukocytosis or in viral infections, a leukopenia.
A. Acute simple gastritis caused by
Differential diagnosis: Includes peptic ulcers and appendicitis.
P. Treat the specific infection or problem. Correct fluid and
electrolyte distia-bance. Place patient N.P.O. until acute s>?nptorris of pain
aid nausea have subided, then start giving clear liquids and progress to a
soft diet as tolerated. Sedatives, Compazine, or opiates may be used as
Indicated. Symptcius last from 1-7 days.
b. Food poisoning and acute gastroenteritis. Food poisoning is a
general tern applied to the sytxJrome of acute anorexia, nausea, vcmitlng,
md/or diarrhea that is attributed to food intake, especially if it affects
a group of people who ate the same foods. There are numerous causative
agents and crganlsms that have similar signs and symptoms to a greater or
lesser degree. The only positive way of differentiating between these
agents or organisms is by culturing the suspected food and stools of the
affected individuals. Jtost forms of food poisoning are self-limiting and
require symptomatic treatment, such as replacement of fluids and
electrolytes, control of diarrhea with Lomotil, and control of nausea and
voniting with Ccopazine. Very rarely patients may develop rtypovolemic
shock and respiratory embarrassment, and this will have to be managed.
Antimicrobial drugs should not be given unless the specific organism can be
identified as they may aggravate the anorexia and diarrhea and prolong the
course of the illness. The exception to the rule is if you suspect
BCrrULISH ; then polyvalent antitoxin must be a<tninTs*t^^. ThenfoTTowing
Chart will help in identifying the various types of food poisoning and
their specific treatments.
C^ganism
Incubation
Period
(Holts) Epidemiology Clinical Features
Staphylococcus 1-18 Staphylococci Abrupt <nset, intense
grow in meats, vciciting for up to 24
dairy, and bakery hours, regular
products and recovery in ?4-48
produce entero- hours. Occurs in
toxin. persons eating the
same food . Mo
treatment usually
necessary except to
restore fluids and
electrolytes.
1-47
1-^8
Clostridlijm 6-16
perfringens
ClostridiiJiB 2^-96
botulinm
Escherichia 24-72
coli (some
strains}
Vibrio p^a- 6-96
haemolyticus
Vibrio 24-72
cholerae
(nUd cases)
Clostridia grow
in rewanoed
meat dishes and
prodLJce
enterotoxin.
Clostridia grow in
anaerobic foods
and produce toxin.
CyganisEs grow
in gLit and produce
toxin. Hay also
invade
superficial
epi thel inn .
Organisns grow in
seafood and in gut
and produce toxin.
Organises grow in
gLtt and produce
tox in .
Abrupt onset of
profuse diarrhea ;
vomiting
occasionally.
IJeeovery usual
without treatment
in 1-4 days. Many
Clostridia in
cultures of food and
feces of patients.
Diplopia, dysphagia,
dysphonia,
respiratory
embarrassreent.
Treatment requires
clear airway, vwiti-
lation , and intra-
venous polyvalent
antitoxin. Toxin
present in food and
sertra. Mortality
rate high.
Usually abrupt
onset of diarrhea;
vomiting rare. A
serious infection in
neonates. In adults,
"traveler's diarrhea”
is usually self-
limited in 1-3 days.
Use diphenoxylate
(Lcnwtil) but no
antimicrobials .
Abrupt onset of
diarrhea in groups
consining the sane
food, especially
crabs and other sea-
food. Recovery is
usually ccxBplete in
1-3 days, food and
stool cultures are
positive.
Abrupt onset of
liquid diarrhea in
endenic area, feeds
prcmpt replacement
of fluids and
electrolytes IV or
orally. Tetracy-
clines shorten excre-
tion of vibrios.
Stool cultures
positive.
24-72
Shigella spp.
(mild cases)
Salmonella spp. B-48
Clostridim
difficile
Campylobacter ?
fetus
Yersinia ?
enterocolitica
Abrupt onset of
diarrhea, often with
blood and pus in
stools; cramps;
tenesmus; and
lethargy. Stool
cultures are
positive. Give
anpicillin ,
chloramphenicol ,
or sulfanethoxazole
with trimethoprim
(co-triinoxazole) in
severe cases. Often
mild and self-
limited. Restore
fluids.
Gradual or abrupt on-
set of diarrhea and
low-grade fever . No
antimicrobials inless
systemic
dissemination is
suspected . Stool
cultures are
positive. Prolonged
carriage is
frequent.
Crug intake, Especially after
e.g-, clindamycin, abdoniiral surgery,
abrupt bloody diar-
rhea and fever .
Toxin in stool.
Oral vancomycin
useful in therapy.
Organism grows in Fever, diarrhea;
jejunum and ileun. P.M.H.’s and fresh blood
in stool, especially
in children.
Usually self-
limited. Special
media needed for
culture. Erythro-
mycin in severe cases
with invasion.
Severe abdaminal
pain , diarrhea,
fever; P.M.N.'s and
blood in stool ;
polyarthritis,
erythema nodosLn,
especially in
children. If severe,
tetracycline or
Fecal-<wal
transmission.
Food-borne.? In
pets.
Organisms grow in
gut. Do not
produce toxin.
Organisms grow in
superficial gut
epi thel itn and
gut lunen and
produce toxin.
1-49
1-30
gentamicin .
c. Bacillary dpentery (^igellosis). Shigellosis is a comcon,
often mild and self-limiting disease that occasionally is serious. It is
usually found in conjunction with poor sanitary conditions.
S. Abrupt onset of diarrhea (often with blood and mucus), lower
abdominal cranps, and tenesmus- This is usually acccanpanied by fe\?er,
chills, anorexia, malaise, headache, lethargy, clouded mental condition,
and in the nnst severe cases raeningismus (S and S of meningeal irritation
without actual infection), coma, and convulsions. As the illness
progresses, the patient beccmes weaker and more dehydrated.
O. Temperature up to 104o F., tender abdomen, and blood, mucus,
and pus In the stool. Stool culture is positive for shigellae.
A. Bacillary dysentery (shigellosis). Differential diagnosis:
Amebic dysentery, salmonella, gastroenteritis, E. coli, viral diarrhea, and
ulcerative colitis.
P. IV fluid and electrolyte replacecoent , place patient H.P.O.;
antispasmodlcs (e.g., tincture of belladonna) are helpful when cranps are
severe. Avoid Lomo til or paregori c; they may improve the general symptoms
but prolong fever , diarrhea , and excretion of shigella in feces- Effective
stool isolation and disposal should be initiated. Drug of choice is
amplcillin 250 q.6h. x 5-7 days; second choice is tetracycline 250 mg.
q.6h. X 5-7 days. After bowel has been at rest for a short tine, start
patient on clear fluids for 2-3 days, then soft diet and gradually build.
d. Amebic dysentery (see Chapter 2, Section T, Parasitic Diseases).
e. Typhoid fever (see Chapter 2, Section III, Bacterial Diseases).
f- Cholera (see Chapter 2, Section III, Bacterial Diseases).
g. Infectious hepatitis (see Chapter 2, Section IV, Viral Diseases),
h. Peptic ulcer disease. An acute or chronic benign ulceration in a
portion of Une digestive tract exposed to gastric secretions.
(1) Duodenal ulcer. ft>st common type of ulcer, four to five
tmies more prevalent than gastric ulcer.
S. Symptoms may be vague or absent. In a typical case pain is
described as gnawing, burning, cratplike, aching, or as heartburn; it is
usually mild to moderate, located near the midline aid near the xiphoid
process. Pain may radiate below the ribs into the back or occasionally to
the right shoulder. Patient may have nausea and may vcmit small quantities
of highly acid gastric juices with little or no food. Usually occurs 45-60
minutes after meals; absent in the morning before breakfast and gets
progressively worse as the day passes. Hay be n»st severe between midnight
and D200. Pain is relieved by food, milk, antacids, and vomiting within
5-30 minutes. Ulcers can spontaneously get better or wrse. Causative
factors nay be unknowi but may include physical or emotional distress,
trauma, or infections.
0. Examination shows superficial »id deep epigastric tenderness,
volintary muscle guarding, and urilaterlaL spasm over duodenal bulb. Lab
gcwk will show occult blood in the stool and anemia in chronic ulcers.
Definite diagnosis depends on X ray and endoscopic examination.
IIqXE; Complications include severe hemorrhc^e due to ulceration into a
vein or artery or even bleeding fran gr^ulation tissue; perforation into
' the peritoneal cavity causing peritonitis; puretration into surrounding
orgws, usually into the pancreas, but the liver, biliary tract or
gastrohepatic cwentun may be involved. In 20 to 25 percent of untreated
patients, minor degrees of pyloric valve obstruction occur, but major or
ccMplete obstructions are rare-
A, Peptic ulcer disease duodenal ulcer. Differential diagnosis:
functional gastrointestinal disease, gastritis, gastric carcincoa, and
irritable colon syndrome,
P, 2-3 weeks rest from work if possible. Relieve or avoid
anxiety whenever possible. Forbid alcohol . Discontinue or avoid drugs
that aggravate ulcers (e.g., phenylbutazone, indonethacin , and Large
aiounts of salicylates). Place patient on a dietary management program.
(a) In the acute phase, start full liquid diet with hourly
antacids liberalized rapidly to a regular diet.
(b) Avoid milk as therapy.
(c) Avoid interval feeding (eating atall meals every few
hours) .
(d) Nutritious diet.
(e) Regular meals.
(f) Restrict coffee, tea, and cola beverages.
(g) Avoid foods that are known to produce unpleasant
synptccts in a given individual.
Antacids, in order to be effective, must be taken frequently. In the acute
phase, antacids should be given hourly. The schedule may then be changed
to a full dose 1 and 3 hours after meals and at bedtinte.
(2) Gastric ulcer. In many respects it is similar to duodenal
ulcer.
S. There may be no symptoms or vague ard atypical symptoms,
rain is epigastric and described as gnawing, burning, aching, or hunger
pangs referred at times to left subcostal area. Usually occurs 45-60
minutes afUr meals and is relieved by fcxxl, antacids, or vomiting. Weight
®ss, constipation, and fatigue are cofrrton.
tK- 7 * c^iigastnc tenderness or voluntary muscle guardir^ is usually
only finding. If there has been bleeding, a guaiac test will show
wccuit blood .
NOTE:
Complications are the same as with duodenal ulcers.
A. Peptic ulcer disease, gastric ulcer. Differential diagnosis:
eoal ulcer, irritable colon, functional gastrointestinal distress, and
1-31
1-52
gastritis.
P. Ireat'Bent is the saiee as for duodenal ulcer. Failure to
respond in 3-4 weeks is it>dication for surgery.
{■astric ulcers tend to be recurrent. Recurrent uncomplicated ulcers
usually heal faster than the previous ulcer.
i. Acute organic intestinal obstruction. Usually involves the small
intestines, particularly the ileun. Major causes are external hernia and
postoperative adhesions. Less ccnnon causes are gallstones, neoplasms,
foreign bodies, intussusception, gr^ulanatous processes, internal hernia,
and vovulus.
S. Colicky abdcminal pain in periimbilical area beccning more
constant and diffuse as distention develops. Vomiting associated witli
waves of pain. If obstruction Is of the distal bowel, vomiting becomes
fecal in nature. Loud stomach growling , unman%eable constipation ,
weakness, sweating, and anxiety are often present.
O. Patient is restless, often in shocklike state with
tachycardia and dehydration, tender distended abdceien (can be localized but
usually generalized) without peritoneal irritation. Audible and visible
peristalsis, high pitched tinkles, and pain related to peristaltic rushes
may be present. Temperature is normal or slightly elevated. A tender
hernia may be present. W.B.C. is normal or slightly elevated.
A. Acute organic intestinal obstruction. Differential
diagnosis: Renal colic, gallbladder colic, or mesenteric vascular disease.
P. Place patient M.P.O. Deccmpress intestinal tract by
nasogastric suction (see illustration on next page). Replace fluids and
electrolytes by IV. Treat the cause of the obstruction. Start
broad-spectrum antibiotic therapy if needed.
j. Appendicitis. One of the most frequent causes of acute abdomen.
Signs and symptoms usually follow a fairly stereotyped pattern, but it cam
display many different manifestations that should be considered in the
differential diagnosis of every case of abdominal sepsis and pain.
S. Appendicitis usually b^ins with generalized periumbilical or
epigastric pain and 1 or 2 episodes of vcmiting. Within ?-1? hours, the
pain ^ifts to right lower quadrant where it persists as a steady soreness
aggravated by walking or coughing. Patient can usually place a finger on s
specific point. Anorexia, malaise, slight fever, and constipation are
usual, but diarrhea occurs occasionally.
0. Rebound tenderness and spasm of the overlying abdcminal
muscles. Rectal tenderness is ccnroon; peristalsis is diminished or absent.
Slight to moderate fever. Pain localized in right lower quadrant, W.B.C.
10-20,000 with an increase in neutrophils.
NOTE: Complications incliide perforation leading to generalized
pieribonitis , appendiceal abscess, pylephlebitis, and Intestinal
obstruction.
BOTTIEI
80TTIE2
1-53
1-S4
A. Appendicitis. Differftitial diagnosis: Acute
gastroenteritis, inesenterlc adenitis, Meckel's diverticulitis, regional
enteritis, anebiasis, perforated duodenal ulcer, ureteral colic, ruptured
ectopic pregnancy, and twisted ovarian cyst may at tines oimic
appendicitis.
P. Place patient under observation for diagnosis within ttie
first 8-12 hours. Bed rest, H.P.O. , start maintaining IV, avoid narcotic
medication as it might mask symptoms necessary for proper diagnosis.
Abdominal and rectal ex an , white blood count, and differential count are
repeated periodically.
fl) Once diagnosis is made, an appendectomy should be performed
as soon as fluid imbalances and other systemic disturbances are controlled,
(2) Antibiotics should be administered in the presence of narked
systemic reaction with severe toxicity and high fever,
(3) Fjnergency nonsurgical treatment when surgical facilities are
not available; treat as for acute peritonitis. Acute appendicitis may
subside and ccmplications will be minimized.
k. Acute peritonitis. Localized or generalized peritonitis is the
most important complication of nuBerous acute abdominal disorders. May be
caused by infection or chemical irritation.
S. Malaise, prostration, nausea, vomiting, fever, depending on
extent of involvement localized or generalized pain and tenderness,
abdcminal pain on coughing.
O. Elevated U.B.C,, rebound tenderness referred to area of
peritonitis, and tenderness to light percussion, over the area- Pelvic
peritonitis is associated with rectal and vaginal tenderness. Spastic
muscles over area of infiaeinatioh . hfhen peritonitis is generalized, there
will be marked rigidity of the entire abdominal wall. This rigidity Is
frequently diminished or absent in the late stages of peritonitis, in
severe toxemia, and when the abdcminal wall is weak, flabby, or obese.
Diminished to absent peristalsis and progressive abdcminal distention is
found. Vomiting occurs,due to pooling of gastrointestinal secretions and
gas. W.B.C. will increase to 10-20, ODO.
A. Acute peritonitis. Differential diagnosis: Peritonitis may
present a highly variable clinical picture and must be differentiated from
acute intestinal obstruction, acute cholecystitis, renal colic,
gastrointestinal hemorrhage, lower labor pneumonia, porphyria, pwiodic
fever, hysteria, and central nervous system disorders’.
P. Treatment is generally applicable as supportive treaticent in
most acute abdcriLnal disorders. TTie objectives are: Control infection;
minimize the effects of paralytic ileus; correct fluid, electrolyte, and
nutritional disorders,
(1) Specific loeasures: Identify and treat the cause; this
usually entails surgery to remove sources of infection such as
appendicitis, gangrenous bowl, abscesses, or perforated ulcers.
(2) General: Bed rest in mediicc Fouler position (sari-sitting) .
Nasogastric <NG) suction to prevent abdcminal distention and continued
LWtil peristalsis returns and patient b^ins passing flatus. Place patient
II p 0. trtil after NC suction is discontinued, then slowly restme oral
Intake* IV for fluid electrolyte therapy and parenteral feeding are
reauired. Harcottcs and sedatives used liberally to insure rest and
Broad-spectrim antibiotic therapy to prevent and control
infections should be initiated. Blood transfusions as needed. Watch
patient for signs of toxic shock and treat as required.
1 , Acute PMcreatitls. A severe abdoninal disease produced by acute
ififiaanatlon in the pancreas and associated "escape" of pancreatic enzymes
into the surrounding tissues. The exact cause is not known, bul more than
80 clinical causes have been related to acute pancreatitis, everything frcK
alcoholism to drugs.
5- Epigastric pain generally abrupt in onset is steady and
severe, made worse by lying down and better by sitting up leaning forward.
Pain usually radiates to the back but may radiate right or left, liausea,
vctiiting, and constipation are present, and severe prostration, sweating,
and anxiety are usually found. There may be a history of alcohol intake or
a heavy meal irined iatel y before the attack.
O. Tender abdcmen mainly in upper abdcmen , usually without
guarding, rigidity, or rebound. Abdcmen may be distended and bowel sounds
■ay be absent. Temperatire of 101 . 1-102. ?Of. , tachycardia, pallor,
hypotension, and a cool clarmiy skin are often present.
Mild jaindiee is common. Upper abdominal mass may be present. Acute renal
failure naay occur early in the course of the disease. W.B.C. 10-30,000.
Urinalysis shows proteinuria, casts in 25 percent of the cases, and
glixxssuria in 10-20 percent of the cases .
A. Acute pancreatitis. Differential diagnosis: Pancreatitis
is hard to tell from coniDon duct stone or perforated peptic ulcer. It must
also be differentiated from acute mesenteric thrombosis, renal colic, acute
cholecystitis, and acute intestinal obstruction.
P. Emergency measures for impending shock: Place patient N.P.O.
If bowel sounds are absent, initiate nasogastric suction. Patient should
be placed at bed rest and given 100-150 mg. demerol SQ as necessary for
^ief of pain. Atropine ruay be given as an antispaancdic 0.4-0. 6 mg. SQ.
Start IV to replace fluids and monitor urinary output. Use shock drugs if
neoessary; calcitan gluconate must be given IV if there is evidence of
hypocalcemia with tetany. Initiate prophylactic antibiotic therapy only if
exceeds 102oF- Patient should be constantly attended and vital signs
checked every 15-30 miunutes. C8C and urinalysis should be done frequently
and monitored.
(1) Follow-up care: Patient should be kept N.P.O. for 48-72
i frequently and closely for evidence of continued
^nawation of the pancreas or related structures. Conduct periodic CBC
irinalysis._ Hyperfeed the patient parenterally for first 48-72 hours,
gradually introduce oral feeding. ItJhen clinical evidence of
**®^eatitis has cleared , place the patient on a low fat diet.
(2) Prognosis: Recurrence is common. Surgery is indicated only
diagnosis is in doubt, if conservative treatment is not working, or in
Pesence of an associated disorder such as stones in biliary tract.
1-55
1-56
Section VI - Genitourinary System
B, Acute CiX)leey3titis. Cholecystitis is associated with gallstones
in ewer 90 percent of cases. It Is caused by a partial or complete cystic
duct obstruction. If the obstruction is not relieved, pressure builds up
within the gallbladder. Prijnarily as a result of ischemic changes
secondary to distention, gangrene nay develop with resulting perforation.
This may cause generalized peritonitis but usually remains localized and
forms a chronic well-c ire inscribed abscess cavity.
S. Usually follows a large or fatty meal. Relatively sudden
onset of severe, minimally fluctuating pain localized in the epigastriin or
right upper quadr^it frequently radiating to infrascapular area. In the
inconplicated case, the pain nay gradually subside over a 12-18 hour
period. Vemiting occurs In 75 percent of cases and 50 percent of these get
variable relief.
0. Right upper quadrant abdoninal tenderness, guarding and
rebound pain. About 15 percent of cases have a palpable gallbladder and 25
percent of cases have jaundice. Fever is usually present. W.B.C- is
usually 12-15,000-
A- Acute cholecystitis. Differential diagnosis: Perforated
peptic ulcer, acute pancreatitis, appendicitis, hepatitis, and pneunonia
with pleurisy on the right side.
?. Place patient K.P.O. Initiate IV for maintenance and
feedir^. Start projiiylactic antibiotic therapy. Give analgesics as needed
(morphine or meperidine). Smooth muscle relaxamts, such as IH atropine or
probanthine, should be used. Patient should be watched closely. W.B.C.
should be done several times a day. Treatment is continued intil symptoms
SLfcside. Cholecystectony is usually required but not as emergency surgery
unless there is evidwice of gangrene or perforation.
i-g6. genitourinary system is made up of the male and female sexual
the urethra, the bladder, the ureters, and the kidneys.
«
GENITOUfilflARY TRAUMA.
a. Kidney traima. Most commonly caused by blunt external force six?h
aS blows, kicks, falls, etc., in the flark area. Other causes are wounds
such as guhshot, stabs, etc.; it is very rarely caused by spontaneous
rupture of a diseased kidney.
S. Pain at site of injury with s boring or tearing sensation
felt in loin or upper abdciaen.
O. Swelling and progressive rigidity of affected side. If there
is a tear in the renal capsule, there is usually a rapidly expanding mass
in the Qank. From -mild to gross hematuria is present in 90 percent of the
cases. Shock occurs in varying degrees. W.B.C. elevates rapidly to 20, OCX)
otd higher.
A. Kidney trauna.
P. Conservervative treatment will usually provide satisfactory
results in most cases where there is no penetrating wound. Bed rest for at
least 2 weeks, until urine is clear. Sh^k and pain measures as required.
Monitor urinary output closely. Patient must force fluids to insure
urinary output of S-'iO ml. /hr. In serious cases, an indwelling catheter
should be installed and throu^ IV therapy provide a urinary output of
25-^0 ml. /hr. Antibiotic therapy should be initiated in all cases as a
prophylaxis. If an infection is allowed to develop, it will cause scar
tissue and further ccmplicatlons. If at all possible, med evac all
penetrating wounds and serious cases.
b. Bladder trama. Causes include crushing injury fnan blows,
seatbelts, etc., particularly if the injury occurs when the bladder is
full;, gin shot or stab wounds; or bony fragments fren fractured pelvis.
S. Severe pain in lower abdomen. Slow and painful iruiation due
to muscle spasm after inji^y.
0- Hematuria, often only a few drops of blood. Progressive
aymptoas of peritonitis depending on the extent of bladder rupture.
A. Bladder traLina.
P- Flat in bed. Treat for shock; install indwelling catheter,
^‘^'^fhylactic antibiotic treatment. Treat related problems (fracture,
etc.).
c. External genitalia traizia. Usual causes are heavy blows, cuts,
®u'eet injury, pelvic fracture, or straddle injury.
^ S. Intense to excruciating pain, swelling, and rapid development
a large hematoma .
*ienaturia
0- Vary with the severity of the condition but will consist of
9 spasnodlc contractions of the vesicle sphincter with pain^ and
1-57
persistent desire to empty the bladder with i/ivoluntary ineffectual
straining efforts artd shock*
A. External genital traima*
P. Indwelling catheter, cold packs, scrotal support, pain
roedication, and treat related problems (shock, wound, etcl .
1*38. GMITOURIJIARY TRACT rMFLAMIATIOtJ.
a. Renal calculi. Caused by a concentration of mineral salts arvd
crystals that ar« formed in the calyx of the kidney. These kidney stones
vary from small sandlike particles to large oval or branching tstaghorn)
stones that may fill the entire renal pelvis. Many factors are
contributory such as infection, obstructions, dehydration, and hereditary
tendency.
S. Severe intermittent colicky pain, radiating to pelvis,
testicle, and/or inner aspect of the thigh. While the stone is in the
kidney, the pain is doll and intensified by motion. When the stone enters
the ureter, a stfdden stab of excruciating pain is felt- If stone is in the
bladder, the patient nay be able to void only in the horizontal position.
O. Usually accornpanled by chills, fever, violent movenents,
sweating, and shock as the stone moves through the Lfreter. Frequency,
urgency, oliguria (diminished amount of urine formation), dysuria (painful
or difficult urination), hematuria, and possibly pyuria (pus in the urine)
are contributory findings. If anuria (complete urinary suppression)
develops, it is indicative of renal failure.
A. Renal calculi-
P. Relieve pain (morphine V4 gr. q.^-3hr>. Relax ureteral
spasms with Pro-Banthine, 1/100-1/150 gr. atropine, or 1/100 gr.
nitroglycerin. Force fluids and keep close record of intake and output.
Strain all urine for stones; these should pass within 2U-36 hours. At the
first sign of anuria this becomes an acute emergency and patient should be
evacuated to a definitive treatment facility.
b. Acute pyelonephritis. An acute infection of the kidney usually
due to an ascending infection (from bladder through ureters bo kidney) but
may start from a systemic bacterial Infection.
3. Sudden onset with chills, fever, some muscular rigidity,
frequency, urgency, and dysuria.
O. Pain on percussion of the back with radiation to
costovertebral angles and along the course of the ureters. L6*inalysis
shows albuBen, pus cells, casts, R.B.C.’s, W.B-C.’s, ^d bacteria. W.B.C.
in excess of 20,00f>.
A. Acute pyelonephritis. Differential diagnosis: Cystitis.
P. Bed rest, force fluids, and soft diet. Eliminate irritants
such as alcohol or cocoa. Antibiotic therapy using Gantrisin,
tetracycline, or penicillin/streptomycin. SjffBptcmatic treatment.
c .
S. Sudden or more gradual onset of burning pain on urination,
often with turbid, foul-snelling , or dark urine; frequency; difficult or
painful urination; and occasionally blood in the urine. Chills and fever
are rare and if temperature is over 100® f . , consider possibility of other
causes than cystitis.
O. Usually no positive physical findings unless the upper tract
is involved. Urinalysis shows pus, bacteria, and occasional hematuria.
W.B.C.’s are rare unless upper tract is involved-
A. Cystitis. Differential diagnosis : Urethritis,
pyelonephritis.
P. Gantrisin (sulfisoxazole) 1 gm q.i.d. x 10 days, alternate
tetracycline 1-? 250 mg. tablets q.i.d. or anpicillin 1-2 250 mg. tablets
q.i.d. Give Pyridii« or roethenanine urinary analgesic. ffOTE: This may
stain urine red to deep orange. Follow up in 2 weeks.
d. Urethritis. Caused by a wide range of agents that include
gonococcus. Trichomonas, E. coli, and staphylococcus.
S. Burning on urination with pyuria. Discharge from urethra
with a consistency from mucoid to purulent.
O. Di.scharge elicited by milking penis. Grao’s stain of
discharge will usually show causative agent.
A. Urethritis. Differential diagnosis: Cystitis, prostatitis.
P. Ensure correct diagnosis with Gran's stain or culture. Treat
causative organism with appropriate antibiotic.
e. Epididymitis. Frequent history of infection elsewhere in the
general area such as urethritis, etc. Strenuous activity may precipitate
spread of the bacteria,
-3. Fever, malaise, nausea, tenderness, and pain that may radiate
to the groin .
O. Inflammation of scrotal skin that may flake or crack.
Scrotum dusky red and warm to the touch. Slight mass in the epididymis.
A. Epidid>TQitis. Differential diagnosis: Orchitis.
P. Bed rest with scrotal elevation. Analgesics for pain,
antibiotic therapy. 1X 3 MO T massage the prostate. If swelling persists,
surgery will be required^
f. O-chitis. Usually results from a ccnplication of murips or other
acute infections.
S. Fever; pain in the groin region.
O. Swelling of the affected testicle (may be bilateral).
A. Orchitis. Differential diagnosis: Epididymitis.
P. Bed rest; suspend the scrotijri in suspensory or toweling
Cystitis. Bladder infection usually due to bacteria.
1-59
1-60
’'bridge” and apply Ice bags. Give codeine or inorphine as necessary for
pain. Inflamiatory reaction can be reduced with hydrocortisone sodiuc
succinate, 100 tog. IV followed by 30 mg. orally q.6h. x 2-3 days. Orchitis
often inakes the patient very uncomfortable but very rarely results in
sterility .
g. F^statltis. Caused by bacterial infection from systemic or
urethral infections. Prostatitis nay be acute or chronic; ovemanipulation
(a lot of sex) of chronic prostatitis gives rise to acute stage symptoms.
S- Acute symptoms: Perineal pain, fever, dysuria, frequency,
and urethral discharge. Chronic symptcits: Lumbosacral backache, perineal
pain, mild dysuria and frequency, and scanty urethral discharge.
O. Acute stage: Palpation of the prostate shows it is enlarged,
boggy, and very tender. Even gentle palpation of the [instate gland
results in a copious purulent urethral discharge. Qironic stage palpation
of the prostate reveals an irregularly enlarged, firm, and slightly tender
prostate. CBC Will often show leukocytosis. Expressed prostatic fluid
shows pus cells and bacteria on microscopy.
A. Prostatitis. Differential diagnosis: Urethritis. Lower
urinary tract infections.
P, Bed rest, force fluids, sitz baths t.i .d. for 15 min,
analgesics, and stool softener.^. For acute prostatitis initial treatment
may consist of sulfamethoxazole 4D0 mg., plus trimethoprim BO mg.
(co-truDOxazole) , 6-8 tablets daily, or tetracycline 500 mg. q.i.d. x 2
weeks or ampicillin 500 mg. q.Mh. x 2 weeks; two-vreek treatment usually
results in subsidence of the acute innamnation , but chronic prostatitis
may continue because most dn^s fail bo reach the prostatic acini. Chronic
prostatitis should be treated with prolonged antibiotic therapy accompanied
by vigorous prostatic massage otx:e we^ly to promote drainage.
S. Obstructive symptoms similar to those of benign prostatic
hyperplasia are ccmon. Low back pain occurs with metastases to the bones
of the pelvis and spine,
0. Rectal exam reveals a stone-hard prostate that is often
mcdular and fixed. Cbstructions may produce renal danage and the symptcros
ajd signs of renal Insufficiency. Urine may show evidence of infection.
A. Carcinana of the prostate. Differential diagnosis: Benign
prostatic hyperplasia, urethral strictis'es, renal calculi, and bladder
tunor.
P. Evac to a definitive care cwJter.
j. Acute glomerulonephritis. Glomeruloneplwltis is a disease
affecting both kidneys. It is most common in children years old.
Host corinon cause is a preceding infection of the pharynx or of the skin
with group AB-hemolytle streptococci .
S. Halaisc , beadacrte, anorexia, low-grade fever, puffiness
around the eyes and face, flank pain, and oliguria (diminished anount of
urine output in relation to fluid intake). Hauaturia is usually noted as
’•bloody" or if the urine is acid as "brown" or "coffee-colored.'*
Respiratory difficulty with shortness of breath may occur as a result of
salt and water retention and circulatory congestion. Tenderness in the
costovertebral angle is ccrmon.
0. Mild generalized edena, mild hypertension, and retinal
hemorrhages may be noted. There may be moderate tachycardia and moderate
to nerked elevation of B.P. The diagnosis is confirmed by urine
examination that taay be grossly bloody or coffee-colored or rnay only show
microscopic hematuria. In addition, the urine contains protein (1-3+), red
cell casts, granular and hyaline casts, sihite cells, and renal epithelial
cells.
h. Benign prostatic hyperplasia. Caused by hyperplasia (abnormal
multiplication or increase in the mnber of normal cells in a tissue) of
the prostatic lateral and subcervical lobes resulting in enlargement of the
prostate and urethral obstruction,
S. Hesitancy and straining to urinate; reduced force and caliber
of the urinary stream, and nocturia. Symptems may be overlooked until the
problem is well developed when the progression of the obstruction is slow.
C. Prostate is usually enlarged on palpation. The bladder may
be seen and palpated as urine retention increases. Infections commonly
occur as retention increases. Hematuria may occur.
A. Benign prostatic hyperplasia. Differential diagnosis:
Urethral strictures, renal calculi, bladder tunor, or carcinana of the
prostate .
P. Relieve acute urinary retention by catheterization. Maintain
catheter drainage if degree of obstrijction is severe. Surgery Is usually
necessary. Treat infections that develop.
i. Carclnorta of the prostate. Rare before age 60. It metastasizes
early to the bones of the pelvis and locally may produce urethval
obstruction with subsequent renal damage.
A. Acute glomerulonephritis. Differential diagtwsis: Other
diseases in Vfhich glouerular inflaonation and tubule danage are present,
P. There is no specific treabnent, but eradication of
EWhemolytic strep is desirable. In unccmplicated cases, treatment is
Sjroptomatic and designed to prevent overhydration and hypertension. Bed
rest until clinical signs abate. Blood pressure should be normal for 1-2
weeks before resuming rtormal activity. When protein excretion has
disminished to near normal and when White and epithelial cells excretion
has decreased and stabilized, activity may be resumed on a graded basis.
Excretion of protein and formed elements in the urine will irKirease with
resunption of activity, but such increases should not be great. Fluids
should be restricted in keeping with the ability of the kidney bo excrete
^■■ine. If edema becomes severe, a trial using an oral diuretic should be
tried.
k- Phimosis.
(1) Cause and symptoms: Foreskin not pliable enough to retract
oyer the gians penis. This causes pain on erection and may be ccmplicated
paraphijDosi s .
(2) Treatment: Cut a dorsal slit in foreskin and schedule for
1-61
circtruoision.
i-b2
Paraphimosis.
(15 Cause and symptoms: Foreskin is constricted around the
glMis penis and cannot he reduced.
(2) Treatment: Cut a dorsal slit in the foreskin and schedule
for circuDcision .
SectioT) VT I - Nervous oystem
1-39. This section is not intended to cover all neurological problems
because most neurological problans are beyond your scope for definitive
treatment. It should, hokvever , provide you with enough information to ir»ke
you aware of the neurological problans you may face and enable you to make
a tentative -diagnosis .
1-iJO. CCHPOSmON OF THF NFRVOUS SYSTEM.
a. The nervous system is composed of (1) Central Nervous System
(C.N.S) - Cerebrum, Cerebellim, Brain Stem, Spinal Cord; (25 Peripheral
Nervous System (P.N.S.) - Peripheral nerves.
b. Review of tlie twelve cranial nerves.
(15 First: Olfactory. Sense of smell. Injury causes loss of
sense of sraell.
(25 Second: Cptic. Sense of sight. Injury causes optic
disturbmces to loss of sight in one or both eyes.
(3) Third: Oculcfliotor . Supplies all the muscles of the orbit
except the superior oblique and external rectus; also supplies the
sphincter muscle of the iris and the ciliary muscle. Injury causes dilated
and fixed pupils, slight prominence of the eyeball, and drooping of the
upper eyelid.
(U5 Fourth: Trochlear. Supplies the superior oblique noscle
(anallest of the cranial nerves5. Injury makes patient unable to turn eyes
downward and outward. If attempted, affected eye is twisted inward causir^
double vision.
(5) Fifth: Trigeminal. Innervates facial sensation and motor
to muscles of mastication (largest cranial nerve) . This nerve also
supplies the eye, nose, teeth, gums, palate, etc." Injury can cause
nuDerous problems from dryness of the nose and eyeball to impaired action
of the lower jaw.
(6) Sixth: Abducens. Supplies the external rectus muscle.
►bre frequently involved in base of the skull fractures than any other
nerve. Injury causes an internal or convergent squint often with a certain
aotount of contraction of the pupil.
(7) Seventh: Facial nerve. Motor nerve of all the muscles of
facial expression: the platysma and buccinator; external ear muscles;
posterior belly of the digastric and stylohyoid; nerve of taste for the
anterior two-thirds of the tongue; the vasodilator nerve of the
SLtMaxiilary and sublingual glands; and tympanic branch supplies the
stapedius muscle. Most conwon effect of injury is Bell’s facial palsy.
(S5 Eighth: Auditory. Sense of hearing. Injury causes
deafness .
(9) Ninth: Glossopharyngeal. Nerve of sensation to pharynx,
fauces, aid tonsil. Also sensation of taste to posterior third of tongue.
(105 Tenth: Vagus. Supplies the organs of voice and
l-W
respiration with motor and sensory fibers and the pharynx, esophagus,
storoach , and heart with motor fibers.
(11) Eleventh: Spinal accessory. Consists of accessory portion
which is motor to larynx arJ pharynx and spinal portion which is motor to
sternooleidonastoid and trapezius muscles.
(12) Twelfth: Hypoglossal, ^y^tor nerve of the tongue.
1-41. RECOCMmON OF KEUROLOGTCAL PROBli?iS.
a. Mot all problems have neurological origin. Your first task is to
recognize the potential neurologic origin of the patient's conplalnt.
There are eight different ccmplaints or problems that point to neurologic
disease. Although each of these complaints may be produced by diseases
that do not involve the nervous system, differentiating between
neurological and non-neyrological causes is usually easy (e.g., a patient’s
leg may not move correctly because it is broken; he can't see properly
because he needs glasses; or he has a headache and fever after taking a
typhoid inmunization) . The eight complaints/problens are:
(1) Something doesn't srove right.
(?) Something doesn't feel right (including disorders of other
sensory modalities),
(3) I can’t see properly.
(h) 3 can't think or ccmmunicate properly.
C5) I have spells.
(6) I am dizzy.
(7) Hy head hurts.
(8) Patient is unconscious, unrousable, or excessively drowsy.
1-42. NEUROLCCIC HISTORY. M>st patients with neurologic disease will tell
their physician is wrong with them if he can properly interpret what
they are trying to say and expands the history with skillful questioning.
The history should give a profile of the disorder. This provides a
valuable clue to the basic disease process. A few general principles are
worth mentioning,
a. Seizures (convulsions) develop more rapidly than any other form of
neurologic disorder. In many cases they develop in less than one second
and may disappear as quickly as they come. Neuralgias are the only other
group of disorders this abrupt. Vascular disorders including stroke and
migraine usLolly take seconds to minutes to develop. Instead of clearing
rapidly they melt away over boirs or days. Demyelination seldocD develops
as rapidly as stroke but may progress over hours to days. Twtors usually
develop in weeks to months and degenerative disorders in months to years.
Toxic, metabolic, and infectious disorders are variable and more likely to
leave their mark on other organ systems.
b. A brief neurologic review of systems should be made. It helps the
medic be sure that the neurologic disorder is restricted to the problem
area he is evaluating. Possible intellectual defects be elicited by
asking about any difficulty in thinking or ranembering, comparing recent
Job or school performaice with past achievements may be helpful, asking
whether he has any difficulty understanding what is said to him or
. expressing himself in oral or written language. . Other possible ccmplaints
relative to the head are logically explored next. These include a
discussion of the patient's headaches. He should be asked about any
spells, attacks of dizziness, or alteration of consciousness he may have
had. Visual complaints including diplopia, scotanata, and loss of visual
acuity should be solicited.
1-43. leUBCLCCICAL EXAHINAIIOM.
a. The following checklist will help you make a neurological
examination: See para b, below, for details,
(1) Mental status.
(a) Affect and mood
(b) Orientation
(c> MefBory
(d) Calculation and abstraction
(e) Aphasia
(2) Patient standing.
(a) Ftoutine gait - note:
2 . Arm swing
2. Width of gait
5- Limp or other abnormality
(b) Toe walking
(c) Heel walking
(d) Tandem walking
(e> Rcnberg’s test
(3) Patient seated on exam table.
(a) Cranial nerve tests:
1. Visual acuity
Visual fields to confrontation
3- Ocular fiMKlus
5. Extraocular movements
5- Pupillary reactions
5. aniling, voluntary and emotional
7. Tongue protrusion
5- Voluntary palate movement
2- Hearing
(b) Arm strength and coordination
2- Strength
a. Shoulder abduction
b. Elbow flexion - extension
c. Thumb adduction
i-6:>
1-66
d, Thunb opposition
e. Wrist dorsiflexion
7- Handgrip
2. JJeflBxes
a. Biceps
E. Triceps
c. Radial - periosteal
3. Coordination
a. finger to nose
b. Rapid alternating Tnovements
c. >*iscle tone
(ij) Patient iying down.
ta) Leg strength and coordination
2- Strength
a. Hip flexion
b. Knee extension
c. Dorsiflexion of the foot
2. Ren exes
a. Abdominal
b. Knee jerk
c. Ankle jerk
d. BEtoinsKi
j. Heel to shin test
(b) Sensory examination
1, Pain
a. Face
b. fxtrCTiities
2. Vibration - extremities
3- 1-ight to\x:h
a . Cornea
b. Face
c. Extremities
b. Position
a. Fingers
b . Toes
b. Further details on neoro'j cgical examination.
(1) Mental status exam. Tne medic who is evaluating a patient's
Tuental status is usually looking for elements of dementia, aphasia,
depression, or anxiety. The.-^e cart often be observed during history taking.
(a) Affect and mood should be observed arid recorded.
Affect is patient transmits his feelings and mood is hhat he is
trying to transmit. In most individuals a depressed affect reflects a
depressed mood and vice versa. Flattening or dulling of affect is seen in
most depressed, schizophrenic, or parkinsonian patients.
fb) Orientation to tinje, place, and person should be
recorded .
Cc) Memory can usually be judged from the Quality of the
history , but should be carmented on. Formal memory testing is unnecess^'y
Lnless there is some reason to suspect difficulty.
(d) Calculation and abstraction should be tested in
patients over 50 years of age. Serial 7’s and a well-known parable {such
as "why shouldn’t people who live in glass houses throw stones?'*) are
usually adequate.
(2) Gait and station. Four types of gait are routinely tested:
ordinary gait , heel walking, toe walking, and tanJein gait. Ordinary gait
is observed for gross abnormalities of carriage and width of base. Arm
swing may be lieficient if there is weakness (especially hemiparesis) or a
basal ganglion disease such as Parkinson's disease. Asyocetrlc heel
elevation during toe walking Indicates weakness in plantar flexors of foot
while asynnetric toe and foot elevation in heel walking suggests weakness
of the dorsiflexion of foot and toes. Tandem walking brings out gait
ataxia (broad-based gait) seen in midline cerebellar disorders. Rcaberg's
test is an evaluation of position sense. The patient is told to stand with
his feet as close together as possible. If, with his eyes open, he can
only stand with a wide base, the problera Is rejst likely cerebellar. If he
stands firm with eyes open, but tends to fall upon closing his eyes, the
problew is position sense (po5t«~ior coiunn or peripheral nerve) and
Renberg’s Sign is present. While performing the Romberg test, it is
convenient to examine for arm drift, a useful test of mild shoulder
we^cness or proprioceptive loss. Before the patiKit closes his eyes, have
h« extend both arms, palms up and elbows stiff in front of him. If while
bis eyes are closed he displays a tendency for either hand to pronate or
either arm to "drift” downward, you may have disccfvered a significant
defect. ft»out 20 seconds of holding against gravity is sufficient,
C3) Cranial nerves. Jiow the patient can be sealed and cranial
nerves tested. Smell and taste need not be routinely evaluated. Vision
requires more attention. Acuity should be checked first. With glasses on,
the ability to read newsprint at about two feet constitutes 20/30 vision;
Wd at 14 inches 20/50 vision. Each eye should be tested separately.
Visual fields should also be tested in each eye sepa»'ately. Always check
all four ciuadrants. In patients over 50 years, check simultaneous
^iwjlation by quadrants, preferably by superior temporal against the
inf^ior nasal and then inferior temporal against the superior nasal. The
optic nerve head is routinely examined as part of the ophthalmoscopic exa^.
A simple tuning fork test for hearing should be included. Extraocular
pi^^illary reactions should always be tested. Etnotional and
iitional face movenents should be observed. Tongue protrusion, volixitary
i« voice timbre should be examLned, but these are
rpfu included as part of the routine oropharyngeal exan. Corneal
Ilexes, Myerson’s sign, and snouting responses should be tested.
s^dsation in the face is best checked later with the rest of the
general sensory exM.
1-67
l-b«
{4) Motor strength and coordination in the upper extreeiities.
Acceptable techniques of muscle testing consisf f
move a joint against resistance or evalictiOT of ^ Mti^t
patient to overcone the exaniner. I generally prefer to have the ^tien
^ert I iiaximin effort against my resistance for i"ternal^d
rotation at the shoulder, flexion and extension of
and extension of the knee. I usually try to Hexion
fixation for shoulder abduction, wrist flexion and extension hip Hex^.
and foot dorsinexion. ■-^hen a' patient is making a maximiin eff^t ^nd ^
exariner is able to overcome the force of his muscle contrition ,_gr^ual
rrovement of the joint will be felt. There should
relaxation, su^esting a lack of full cooperation. T^e
numerical and descriptive scales for recording «e^ess. Like ^scriMng
unconsciousness as ccma . semicona. and lethargy . they
consensus amor« physicians as to ^at the n^.bers th*s
the examination, shoulder abduction, eltow
dorsi flexion, and thumb opposition and adduction should be tested
bilaterally. Biceps, triceps, and radial-periosteal reflexes may be tested
at ms time or deterred urtil the patient is
muscle tone should be checked. Three maneuvers are essential, m tirs
is the familiar finger to nose test. While this is being
any trecDor or involuntary movement. Rapid alternating
either of opening and closing the hands or touching the ^
with the tip of the thunb is tested next. Finally, passive other
Of each wrist should be tried while the patient o^ns and
hand as fast as he car. IMs will bring out any latent musc.e rigidity.
(5) Cocpletion of the motor and reflex exEin. The patient should
now be placed in the supine position. Up to this . .
deliberately sloppy in testing strength. ’We have be^ "i-
providing fixation of the limb. As a screening procedire, this iS fine.
If any weakness nas been suspected, Moulder rotation and elbw movCTents
should be retested with the shoulder fixed against the ' .
Wrist and hand movements can similarly be isolated.
extension of the knee, and dorsiHexion of foot
exaeined. If there is a question of knee weakness, have the
the prone position, fix the thigh against the table, and retest flexion and
extension.
Biceps, triceps, and radial-periosteal reOexes i" the am
be tested if they have not beer previously. Knee jerks, '
abdominal renexes should be tested, and Babinsjd^s sign
reflexes require three elements: a sensory lifob, seme form of central
integration, and a motor response. Reflexes will be ^ -
these three elements are disturbed. Any peripheral s^^ry
disturbance of the lower motor neuron or '^’^scle can abolish regexes. T^
wily thing that will exaggerate reflexes is a disorder of the corticos^
system (the upper motor neuron syndretne) . Finally, leg coordination should
be observed with the heel^t^shin test*
(6) Sensory exm. It is corvenlent bo perform the entire
sensory e*am at one time with the patient lying supine* ^ring ^ ^
screening exan, pain sensation with a sharp pin and fine touch with a wi^p
of cotton or Kleenex should be checked on both c^ks, both hands, and
feet- tosition sense should be tested at least in the toes, and vibra
sense in both feet and hands . A tuning fork should be used to test
vibratory sensation on bony prominer>ces.
1-<IA, EPILEPSI, Any recurrent seizure pattern. Violent, involuntary
contractions of the muscles, occurring singly or in series, often
acccxBpanied by sudd^ loss of consciousness.
a. Grand mal attacks.
CD Focal or jacksonian seizu-es. Initiated by specific focal
phenomena Cmotor or s«i3oryj. Seizures are one-sided or localized. Head
and eyes may turn to one side (that opposite the lesion). Jerking cf the
licbs may be one-sided. This is an acquired type of epilepsy. Convulsive
movemOTts start in sinaLl mosele groups (e.g., the hand) and slowly spread
to other areas, it is terrned the jacksonian ’'march." Loss of consciousness
results shen it beccoes a generalized convulsion. Indicates specific
portion of the cerebrum where lesion is located. May have an "aura," oftKi
referred to as a warning, but in reality it is a part of the seizure. The
focal point indicates area of the brain where attack originates. Should be
considered the focal trigger for the seizure.
(2) Typical grand mal seizures are characterized by a cry; loss
of consciousness; falling; tonic then clonic muscle contractions of the
extremities, trunk smd head; urinary and fecal incontinence; frothing in
the mouth; biting of the tongue. About 50 percent have an aura (auditory,
visual, olfactory, visceral, or mental) disturbance. Losing consciousness
after crying out, the person falls making no effort to protect himself.
(a) Tonic phase: sustained contraction of all muscles;
body is rigid, jaws fixed, hands clenched, l^s are extended, dilated
pupils, face is red or cyanotic due to spasm of respiratory muscles.
(b) Clonic phase follows tonic phase in less than a minute
with jerky movements due to alternating contraction and relaxation of
muscles. The attack lasts 2 to 5 minutes usually. These attacks may be
followed by deep sleep, headache, or muscle soroiess .
b. Petit mal attacks. Fleeting attacks of staring into space without
loss of consciousness (absence attack) for 1 to 30 seconds. Can occur with
loss of muscular tone. Occurs predcninantly in children and can recia- as
frequently as 100 attacks per day. Petit mal may eventually develop into
grand mal later in childhood or adolescence.
c. Status epilepticus (continuous seizures).
(1) A serious condition in i*ich seizures of the grand mal type
follow in rapid succession with no intervening period of consciousness.
(2) TreatJDent of this particular condition: Give sodiun
phwiobarbital (Lunlnal) 0.4 to 0.6 gm or paraldehyde 3 to 6 ml .
intravenously to produce brief anesthesia and to help prevent further
attacks.
d. Psychomotor seizures do not conform to the classic criteria of
grand mal, petit mal, or jacksonian seizures. These are minor seizures
with loss of contact with environment for 1 to 2 minutes. The patient does
hot fall but may stagger around performing autcroatically and does not
wderstand k*iat is being said. He may resist aid- Mental confusion
continues for 1 to 2 minutes after attack has ended. Hay develop at any
age. Usually associated with brain danage.
1-69
1-70
e. Trpatjnert of convulsive seizures*
(1) Prevent the patient from injur iriR himself by placing a
tongue depre^'ssor* harvdkerchief or padJed Rag betwesTi teeth to prevwt
bitlne of the tongue. Do not restrain patient. Do not leave him alo^.
If possible, before seizure, place a gag betijeen th& ^eth, but use
a cuetal object. Do not pry the teeth open. Loosen clothing, es^a^
ETOind the necK. Turn bead to the side, allowing mucus to flow from mouth
and throat. After the attack, give phenobarbital 15-30 mg. t.l.a.
* 2 ) Patient should be bospitalized . If hospitalization is iiot
mssible vou will have to control the seizures usir« anticonvulsant drugs
rjhis ICO „g. t-i-d. to q.i.d. P.O. or IK. If
pt«nobarbital 15-30 mg- t.i.d. to q.i.d. What yoo is the
possible to prevent seizures. To accomplish this start «th a
and if the patient has another seizure add a little to the
seizures disappear completely. Patient must not drink alcohol-
1-H5. HTSTERICAL ATTACKS VS. GRAND WL ATTACKS.
a. May resemble grand mal epilepsy. With hysterical attacksthe
onset is slower and movements are purposeful, incontlnOTce ^ ^
^sent, pupils do not dilate, patient does not injure himself fc*ien
falls, dMS not bite his tongue, usually has history of emotional upset and
neurosis *
b. Treatment is the same as (1j of epilepsy treatii^t.
1-46- BEIL'S PALSY. A paralysis of the muscles of one side of the face
sometimes precipitated by exposure, chill, or traima. Can occur at any age
but ROSt cowTiDn fron 2D-50.
S. and 0- One side of the face sags — eyelids, lips, eyebrouis, or
entire face.
A. Bell ' s palsy.
P. Keep face warm aid avoid further exposure, especially to wind
dust. Protect eye with patch if necessary. Gentle upward massage of
the involved muscles 5-10 minutes 2-3 times a day helps maintain
tohe. Prednisone 40 n^. daily x 4 days, then taper to 6 mg. a day m o
days may help. In most cases partial or c<»plete recovery occurs usually
in 2-8 weeks ( 1-2 years in older patientsj .
Section VITI - The Endocrine System
1-47- The endocrine system is made up of glands of internal secretion
(ductless glands). The secretions (hormones) enter directly into the blood
or lymph circulation. Very small quantities of horrtones ^e produced, only
a trace being necessary to produce an effect, and some of them influence
the body as a whole- Because of this and the fact that endocrine disorders
can mimic a wide variety of primary disease states, the diagnosis of
endocrine diseases is extremely difficult to make. The hontione prodicing
glands include the pituitary, thyroid, parathyroids , ardrenals, gonads, and
pancreas .
1-48. GOITEJ? (see Chapter 5i Nutritional Diseases and Deficiencies) .
1-49- DIABETES MELLITUS. A chronic metabolic disorder, characterized by
abhoraal Insulin secretion a-vj a variety of metabolic and vascular
manifestations reflected in a tendency toward ^normally elevated blood
glucose levels, large vessel disease, nicrovascular disease, and
neuropathy -
S- Polyuria, increased thirst and hunger, paresthesia, and
fatigue. Bed wetting may signal the onset of diabetes in children.
Vaginitis and pruritus vulvae are frequent initial complaints of adult
females. There may be narked weight loss despite normal or increased
appetite. Diabetes should be suspected in obese patients, patients with a
positive fanily Hx of diabetes, and in women who have delivered large
babies (over 9 lbs) or have had unexplained fetal losses.
O. In mild or axjderate diabetes there may be no abnormal signs
at onset, whereas the patient with severe insulin deficiency may present
with loss of 5Q fat, dehydration, muscle wasting, anorexia, nausea,
vcmiting, air hunger, and if untreated, ccma death. The retina may
show tnicroarwuryans, intraretlnal hemorrhages, and hard exudates.
Cardiovascular signs include signs of circulatory embarrassment of the
lower extremities and hypert«ision. teurologicai si^s are predcraihantly
sensory in nature with dulled perception of vibration, pain, and
temperature, particularly in the lower extremities. The ankle Jerk is
often absent, but the knee Jerk may be retained. CVinalysis is positive
for glucose and ketones with specific gravity t.02u-1.D40. NOTE: Certain
ecnmion therapeutic agents, e,g., ascorbic acid, salicylates, methyldopa,
and levodopa, when taken in large doses, can give a false positive for
glucose uhen using Clintest measurements or false negatives when using
glucose -oxidase paper strips (Clinistix, Tes-Tape, etc.). Despite the
importance of the sttove signs and symptoms to the diabetic syndrome, none
constitute the basis for a conclusive diagnosis. Whenever diabetes is
suspected, it should be confirmed by a fasting blood or serLin glucose and a
glucose tolerance test if indicated.
A. Diabetes meliitus. Differential diagnosis: Nondiabetio
(renal) glycosuria, hyperglycemia due to end organ insensivity to insulin.
P. A well b.alo,iced (sugar free) 1,000-1,200 calorie diet md
weight reduction will manage many cases of mild to moderate diabetes,
especially in obese patients who demonstrate s^mptcfnatology at age 40 or
above. If glycosuria persists, the use of hypoglycemic agents such as
insulin or tolbutamide (Oranase) is indicated. The ultimate choice of
agents, route, dose, and interval must be detennined by a careful analysis
of serun glticose levels.
1-71
1-72
1J50. COnPLICATIIJKS Cf DIABETES.
a. Hypc^lycetnia (insulin shock). An abnomally low blood sugar level
and the mos^onmon complication of patients on insulin therapy.
S. Sudden onset (slower with long acting insulins) of mental
oonfusion, bizarre behavior, sweatir^, palpitations, and trcfnulousness tha
may lead to coma, convulsions, and death.
0. air. is iTBist. pale, and cool. There may te doling frOT
tbe mouth- Respirations are nonnal or shallow and the ^eath is i^uaily
odorless- B.P. is nomal with a full bounding pulM. urine
Native for glucose and ketones by tbe second voiding (there
resld^ from earlier hyperglycemia.) Ser..™ gluoome 15 <60 mg./lOO
ml.
A. Hypoglycania due to insulin reaction. Differential
diagnosis: Diabetic ketoacidosis, alcohol or drug induced
inSry, and cerebrovascular accidents. NOTE: If serin glucose is <50
n^./lOO ml. the Dx is confirmed.
P. If still conscious and able to swallow, give orange juice,
glucose, or any beverage containing sugar. If stuporous or unconscious
give 20-50 tDl- 50* glucose IV stat. Then continue i"f>J5ion at a °f 10
an/hr If patient is still hypoglycemic, give a second bolus of 25 nl* 50%
^ose. iriiiable to start IV, give 1 mg. glucagon IH or SO then st«ar by
mouth when patient is awake and can swallow. If neither glucose nor
glucagon is^lvailable. give 30 ml. syrup or honey m 500 [nl.
rectaliy. Monitor patient response and plasma glucose level carefully.
b. Diabetic ketoacidosis. Hyperglycemic coma. Usually occurs in
insulin depefxlent and juvenile (age <3°) onset diabetics.
S Gradual onset (1-2 days). Nausea, vciuiting, abdcmiinal pain,
polyuria, intense thirst, arwJ (Barked fatigue progressing to rnental stupor
and finally coma ^ death, if untreated.
0. Skin is hot, dry, and flushed with a loss of turgor.
is dry. Respirations are deep, rapid, and labored. A fruity
odor is usually present on the breath. There may be signs of shock isee
^ter 15). The eyeballs are soft. l>-ire glucose and ketones are
strongly positive. Plasma glucose is >300 mg./lOO ml. and ketones ^e
strongly positive. NOTE: A rapid blood glucose rieterrainati^ cw be made
using c^rcially available glucose test strips (Dextrostix) and a rough
ctu^titation of serin or plasma ketone can be made ^Jing eit^r Ketostix
Acetest tablets. The presence of ketone may be masked if there is a strong
level of lactic acid present.
A, Diabetic ketoacidosis. Differential diagnosis:
Hvpcfilycatia, lactic acidosis due to septic, cardiogenic, or hy^oleaic
shock. MOTE: With lactic acidosis, the clinical picture will be
approximately the sane without the acetone breath or ketonuria. Blood
glucose is variable.
p (1) Diabetic ketoacidosis. Start IV -5 N saline at rate of
1 L./hr X ? hrs, them adjust to 5-8 L. (total) over a period of f tours.
If patient is already in shock, give N saline. Insulin (regular) 5-1u
units/hr slow IV drip or When blood glucose i-s <250 mg./lOO ml., start
IV D5W at a rate of approximately 200 nl./hr witl*i insulin q.2-Nh. p.r.n. to
(•alntain glucose level between 200 and 250 mg./lOO ml.
{?.) Lstttic acidosis. Start IV .5 N saline at rate of l L./2
hours, th»i t L./2-3 hours. Ma bicarbcviate 2 ampules (90 roEq.) stat.
» }iepeat with 3 -tj anpules if necessary. Stop when breathing returns to
nomal .
c- Prevention of soft tissue ccnplications. Diabetics are
susceptible to bedsores, infection, and gangraie. Because of poor
circulation, feet should be kept scrupulously clean and dry. Extreme care
should be used >^en triimiing toenails, and corn and callouses should be
removed by soaking, not cutting. Use oil or lanolin to keep feet soft and
avoid tight shoes. Co not apply local heat to legs and feet. Instruct the
patient to brush teeth at least three times a day. Take warm baths dally
awl seek prcnpt attention for any bruise or break in the skin.
1-51. JUIUTE adrenal I)iSUFFICIENCY. A clinical syndrome caused by marked
deprivation or insufficient supply of adrenocortical hormones following
trauma, surgery, overwhelming sepsis (principally meningococcemia) , or
sudden withdrawal of corticosteroid drug therapy. Acute adrenal
ijiKifficiency constitutes a grave medical emergency and is rapidly fatal if
not treated .
S. Headache, lassitude, nausea, voniting, abdominal pain, C.V.A.
pain, and tenderness. Confusion or ccma may be present.
O. Fever ID 50 F. or more, B.P., cyanosis, petechiae (especially
with meningococereia) , dehydration, abnormal skin pigmentation, and
lymphadenopathy marked eoslnophilia. MOTE: A high eosinophil count in the
presence of severe stress due to traLfoa, infection, or other mechanisms is
strongly suggesti ve of adrenal failure.
A. Acute adrenal insufficiency due to .
Differential diagnosis: Diabetic ccma, cerebrovascular accident, acute
poisoning.
P. IF ADRENAL FAILURE IS SUSPECTED, TftEAT AT OWCE rilTHCOT
WAITING FOR CONFIRHATIOK BY UB RESULTS. Treat for shock (see chapter 15).
Start IV fluids stat., vasopressor drugs and O 7 P-r.n. Do not give
narcotics or sedatives . 100 rag. Solu-Cortef Iv stat. and cantinue IV
infusion o^'~5O-10D mg', -q.bh. x 1 day, then same amount q.3h. x 1 day.
Continue to give q.8h. with a gradual reduction in dose until the patient
is able to take food by o>outh, then give oral cortisone 12.5-25 mg. q.6h.
and reduce to maintenance Levels p.r.n. Monitor B.P. and observe for signs
of edema and hypertension- If signs of cerebral edema (uncon.sciousness or
convulsions) or puLncHiary edema occlt, withhold sodium and fluids and treat
ii>ese conditions. If signs of hypokalemia occir, give potassiun salts or
food high in potassiLin content (orange juice or baianas). Evacuate i*ien
feasible.
i-?3
1-76
Section IX - Eye, Ear, Nose, and Throat (EElfT)
1-52. EYE DISORDERS.
ConjLnctivitis. CorjL^ctivitis is tte most common ^ It
may be acute or chronic. Most cases are due to bac^ial , ^
chlamydial infections. Other causes are allergy,
fur^al or parasitic infection. The mode of trananission is usually direct
contact via fingers, towels, etc.
a. Bacterial conjunctivitis.
S. Copious purulent discharge and redness with no pain or
blurring of vision .
O. Gran's stain of discharge usually shows streptococcus or
staphylococcus oi^anisns.
A. Bacterial conjunctivitis, ^differential diagrosi^ IriU
glaucoma, corneal traima, keratitis, and other causes of conjunctivitis.
P. Disease is usually self-limiting, lasting
ijjtreated. Sulfonamide or antibiotic ophthalmic ointment applied locally
t.i.d. usually clears the infection in 2-3 days,
b. Viral conjunctivitis.
S, Redness, copious watery discharge, and scanty eiixJate frOT
the eye. Lteually associated with systemic symptons , pharyngitis, feve ,
malaise, and adenopathy.
0. Children are more often affected. Contaminated swimming
pools are a major cause.
A. Viral conjunctivitis. Differential diagnosis; See bacterial
conjunctivitis ,
p. No specific treatment. Lfse antibiotic ophthaLmic ointment to
prevent secondary infections. Usually lasts at least 2 weeks.
c. Chlamydial keratoconjunctivitis (trachoma) . J ,
cause of bUodness. In ebdanic areas U le
usually insidious with minimal symptoms. In adults it is acute.
s. Redness, itching, tearing, and slight discharge .
O. Bilateral follicular conjurKitivitis, inflammation of the
cornea, and parwus (cloudy, uneven, newly formed vascular tissue over the
cornea). In the later stages, scarring of the eyelid cau^
inversion of the eyelid and the eyelashes causing th^ to rub against the
cornea thereby scratching and scarring the cornea. This
vision, leading to blindness. Ciensa stain scraping from cc«junctiva shows
typical cytoplasmic inclusions in the epithelial cells. In active
tf-Khoma, the anear may also include polymorphonuclear leukocytes, plaana
cells, and debris-filled macrophages.
A. Trachcma, Differential diagnosis: Other eye infections.
P. Cral tetracycline 250 mg. q.bh. x 3-5 weeks, good hygiene
practice .
1-53. EAR DISORDERS.
a. External otitis. An infection of the external ear canal, usually
bacterial, with occasional secondary fungal infection. In meny cases there
is no infection; it is a contact dermatitis or a variant of seborrheic
derma titls.
S. Itching and pain, dry scaling ear canal; there may be a
hetery or purulent discharge and intermittent deafness. Pain may became
extreme when ear canal becaues completely occluded. Adenopathy and/or
fever indicates increasing severity of infection.
0. Crusting, scaling, erythema, edema, and pustule formation.
Cerunen may be absent. Lab: W.B.C. may be elevated or normal.
A. External otitis. Differential diagnosis: training otitis
media .
P- Clean ear, then apply antibiotic ointment or ear drops with a
cotton wick for 24 hours, follow^ by ear drops twice daily. If there is
systemic involvement, systemic antibiotics nay be necessary.
b- Otitis media. Infection of the tciddle ear.
(1) Acute otitis media.
S, Ear pain, deafness, fever, chills, hearing loss, and a
feeling of fullness and pressure in the ear. If the eardrum ruptures,
discharge is found in the ear.
O. Exam shows a loss or normal landmarks and a bulging of the
eardruB as the pressure increases. Lab: W.B.C. usually increased; Cram's
stain of drainage may reveal infecting organism.
A. Acute otitis media. Differential diagtx>sis: External
otitis, chronic otitis media.
P. Bed rest, analgesics, and systemic broad-spec trun
antibiotics. Ear drops are of limited value; local beat may help resolve
the infection, (tost important is a myringotomy (Incision of the tympanic
membrane) if there is continued bulging of the eardrun, continued pain,
fever, increasing hearing loss, or vertigo.
(2) Serous otitis media,
S. Hearing loss, full or plugged feeling in the ear, and an
unnatural reverberation of the patient’s voice.
0. EardruB retracted often with a characteristic "ground glass"
atoer discoloration. Air-fluid bubbles or a fluid level can scmetimes be
on the eardrum. Absence of fever, pain, and toxic symptoms. Serous
otitis media is caused by eustachiar tube blockage.
A. Serous otitis media. Differential diagnosis: Acirte otitis
media.
1-75
1-76
P. tesal decongestants to keep eustachian tube open.
Antihistamines if there is any suggestion of nasal allergy. Treat cause of
blockage, e.g-, tonsillitis or sinus infection. If all else fails to
relieve the fluid, a m/ringotoiiy is necessary to drain the ear. Indwelling
plastic tubing for drainage can be used in persistent cases.
c. Diseases of the inner ear.
M) Meniere’s disease. Characterized by recurrent episodes of
severe vertigo associated with deafness and tinnitus. M^iere's disease is
usijally encountered in men LO-60 yrs old. Cause is not known.
S. Intenaittent severe vertigo that may cause the patient to
fall. Nausea, voniting, and profuse perspiration are often associated.
These attacks may last from minutes to several hours. Frecfuency of attacks
varies, headache, heari
…[truncated]