TREATMENT
OF
THE
CRITICALLY
ILL
CHILD:
HEMORRHAGIC
SHOCK
Robert L. Replogle, M.D.
Department of Surgery, Sections of Pediatric and Thoracic and Cardiovascular Surgery,
Pritzker School of Medicine, University of Chicago, Chicago
Supported by the Office of Naval Research Contract #N00014-67-A-0285-005.
ADDRESS FOR REPRINTS: 950 East 59th Street, Chicago, Illinois 60637.
DIAGNOSIS
AND
TREATMENT
S
HOCK in the child is nearly alwayscaused by blood
(
or fluid) loss, burns,or infection. The goal of the physician is to
recognize which of these are causing shock
in his patient, and to treat both the
under-lying disorder and the shock as quickly as
possible. This review will touch only on the
clinical management of the patient in
hem-orrhagic shock.
The pathophysiology of hemorrhagic
shock is characterized by a decrease in
car-diac output resulting in inadequate tissue
perfusion, tissue hypoxia, and acidosis; and,
it is caused by an inadequate circulating
blood volume.
The patient often arrives in the
emer-gency room with multiple injuries, being
hypotensive, tachycardic, tachypneic, and
obtunded. First priority is given to
estab-lishing an adequate airway, stopping
mas-sive hemorrhage
(
application of manualpressure or tourniquets
)
, and splintingunstable fractures. Since many resuscitative
measures should be undertaken
simulta-neously, even the most experienced
physi-cian should call for assistance as soon as he
recognizes the seriousness of a patient’s
condition. The nurse should start a chart on
the patient, recording at frequent intervals
vital signs, pupil size and reaction, and
fluids and medications given. As quickly as
possible, one or more routes for the rapid
infusion of fluid should be established. In
the child this is best accomplished by
cut-down of the greater saphenous vein at the
ankle and insertion of a large bore
catheter.’
(
Efforts at introducing a needleor catheter percutaneously into a collapsed
peripheral vein will usually waste valuable
time.
)
Vasopressor or cardiotonic drugs arerarely used in the treatment of shock, but
there may he a specific need for them early
in resuscitation while blood volume is being
rapidly restored. If no blood pressure or
pulse can be obtained, but heart sounds can
be heard or an ECG shows electrical
activ-ity, it is better to use calcium gluconate
and/or epinephrine to temporarily sustain a
heart beat than to delay and risk cardiac
arrest. Sodium bicarbonate solution should
be used extensively to treat the acidosis;
and, until arterial samples can be obtained
for pH measurements, two or three
infu-sions of 1 mEq/kg should be given
empiri-cally.
While blood is being set up for
transfu-sion, replacement of the volume deficit
should be undertaken with some type of
plasma expander. There are differing
opin-ions about the type of fluid to be used
mi-tially while compatible whole blood is
being prepared, but all agree that some
type of volume replacement should be
started immediately. Blalock2 observed that
it is the restoration of intravascular volume
that is of primary importance in
hemor-rhagic shock; replacement of the red cell
volume is of secondary importance. There
may even be some hemodynamic benefit of
moderate hemodilution in shock.3 Colloid
plasma expanding agents appear to be
preferable, since it is possible to predict the
degree of volume expansion from the
amount of fluid infused. Among these, a
commercially available plasma-like material
consisting principally of 5% serum
albu-men is quite satisfactory. Despite the
wide-spread enthusiasm for low molecular
weight dextran, there is little solid evidence
that its usefulness extends beyond a volume
replacement effect; furthermore, low
molec-ular weight dextran leaves the vascular
space rapidly: as much as 50% of the
in-fused volume may be lost extravascularly
DIAGNOSIS AND TREATMENT 1047
within two hours. ‘ The so-called “clinical
dextran”
(
molecular weight 70,000)
is aneffective plasma expander; but, if it is given
in large quantities
(
over 1,000 ml in anadult
)
, it may exert a deleterious effect onthe coagulation mechanism.6 As soon as
blood is available it should be used unless
there is evidence of hemoconcentration
(
hematocrit greater than 40%),
in whichcase a non-sanguinous material is
prefera-ble.
If the Iatient is bleeding massively, it is
not wise to wait until the hypotension has
been completely overcome by fluid infusion
l)efOre initiating efforts to control the
source of hemorrhage. Rapid infusion of
fluid can be continued while the operating
room is being prepared and the patient is
taken to surgery. The suspicion of major
in-tra-abdominal or intrathoracic hemorrhage
can be confirmed by a diagnostic tap, for
which an 18 gauge needle and 10 ml
sy-ringe is used to aspirate the four quadrants
of the peritonea! cavity and both pleural
cavities. The presence of large amounts of
blood in the peritoneal cavity is an
indica-tion for early surgical exploration.
Hemo-thorax, on the other hand, can usually be
managed by the insertion of a chest tube
p05-teriorly through the seventh intercostal space
on the affected side and attaching it to
chest suction bottles. Continued recovery of
large amounts of blood from the chest tube
is reason for thoracotomy to control
bleed-ing.
When it is apparent that immediate
sur-gery is not indicated, and while adequate
volume replacement is underway, the
pa-tient can be evaluated more thoroughly.
Chest and abdominal x-rays, urinalysis, and
a hematocrit are the basic laboratory
stud-ies. Physical examination should focus
par-ticularly Ott abdominal tenderness to deep
palpation
(
especially over the spleen),
agood neurological evaluation, and careful
as-sessment of the extremities and ribs for
pos-sible fractures. Special studies may include
intravenous pyelography or cystography if
kidney or bladder injury is suspected, and
skull and extremity x-rays; selective
angiog-raphy may be very useful in certain
circum-stances to delineate specific arterial injuries.
The patients can generally be separated
into two distinct groups rather quickly. One
group includes those without evidence of
major organ damage, neurological
impair-ment, or displaced fractures, in whom the
vital signs stabilize quickly following
moderate transfusion. The others
consti-tute the more severely injured; they
fre-quently require emergency surgery and
represent complex problems in resuscitation
and management.
For all patients the constant attendance
of a good nurse and frequent visits by an
interested physician are imperative to
per-mit early recognition of an unfavorable
change in condition. The standard methods
for evaluating the adequacy of the
circula-tion are satisfactory to monitor the patients
less severly injured, i.e., blood pressure by
cuff, heart rate, temperature and color of
the extremities, time required for capillary
refilling of the fingers and toes, and so on.
However, the massively injured patient
may present some very difficult problems,
and the physician is well advised to obtain
all the physiological information possible.
Since an accurate l)lood pressure may he
difficult to obtain by auscultatory methods,7
and frequent arterial blood samples may he
required to measure pH, pCO2, and pO, it
is very helpful to have an indwelling
arte-rial catheter. This is most easily done by
cut-ting down over the radial artery at the
wrist and inserting a small catheter
(
PE 50is large enough
)
under direct vision. Withcare and frequent irrigations with
heparin-ized saline, patency’ can be maintained for
prolonged periods even in the smallest
in-fant.
The central venous pressure
(
CVP)
mea-surement has become virtually a necessity
to evaluate properly the adequacy of
vol-ume replacement in hemorrhagic shock.8
This is particularly true in children since
cardiac “pump failure” secondary to
coro-nary artery occlusive disease is not a
con-sideration. The resuscitative effort in
hemor-rhagic shock is directed toward restoring
cardiac output, and since the contractile
1048 HEMORRHAGIC SHOCK
the diastolic filling pressure (or volume),
increasing this pressure by raising the
cen-tra! venous pressure
(
through volumeinfu-sion
)
will increase myocardial contractilityand cardiac output. This is predicated on
the knowledge that central venous pressure
and left atrial pressure are equivalent
(which is nearly always true) and that the
left ventricle is not failing (which is
un-likely in the otherwise healthy child
)
. TheCVP is usually measured by means of a
catheter threaded into the superior vena
cava, either percutaneously or by cutdown.
It is often imprudent to be specific about
levels of pressure to be maintained; but, as
a rough although useful gauge, fluid or
blood may be infused safely without need
for concern about pulmonary edema as long
as the CVP remains below 20 cm H,O. It
would he very unusual for the child in
shock secondary to blood loss to be
hypo-tensive with a CVP of 15 to 20 cm H2O
un-less there were some complicating issue
such as hemopericardium, septicemia, or an
unrecognized cardiac lesion. Like many
useful techniques, there is a tendency
to-ward a ritual-in this case the ritualistic
order would read, “infuse volume until the
CVP goes above 15 cm H20.” If the patient
is clinically doing well, has a good blood
pressure and full pulse, a good urine
out-put, and so on, there is no need to maintain
the CVP above a level at which he is
ob-viously hemodynamically sound, be it 1 cm
1120 or 15 cm H2O.
A Foley catheter inserted aseptically into
the bladder is a very useful adjunct to help
gauge the adequacy of volume replacement
on an hour-to-hour basis. The patient with
a satisfactory cardiac output
(
thus renalperfusion
)
will continue to make urine at asteady rate. In the child this volume can be
as little as 5 ml per hour temporarily.
How-ever, the presence of a urinary osmolality of
300 to 400 mosm per liter and a urinary
so-dium concentration greater than 50 to 60
mEq per liter in an oliguric patient give
cause for grave concern that the oliguria is
secondary to acute renal failure. In some
instances, the infusion of a test quantity of
hypertonic mannitol
(
20% concentration)may help separate the patient oliguric from
hypovolemia or water deficit from the
pa-tient oliguric because of renal failure, since
the first group of patients will respond to
the mannitol infusion with a brisk diuresis.
This author is not convinced that many
pa-tients have been spared the onset of acute
renal failure by the sustained infusion of
hypertonic mannitol during the period of
resuscitation from hemorrhagic shock, and
the obligatory diuresis that often does occur
when mannitol is given eliminates an
other-wise useful measurement for the evaluation
of an adequate volume replacement, i.e.,
the level of urinary output.
Used in conjunction with the clinical
evaluation, the arterial blood pressure,
cen-tral venous pressure, and urinary output are
the most valuable guides to adequacy of
volume replacement in hemorrhagic shock,
and it is volume replacement that is the
name of the game for the treatment of
hem-orrhagic shock.
REFERENCES
1. Randolph, J.: Technique for insertion of a
plas-tic catheter into the saphenous vein. PEDIAT-RICS, 24:631, 1959.
2. Blalock, A.: Principles of Surgical Care. Shock
and Other Problems. St. Louis: C. V. Mosby Company, p. 158, 1940.
3. Replogle, R. L., and Merrill, E. W. :
Flemodilu-tion: rheologic, hemodvnamic and metabolic consequences in shock. Surg. Forum, 18:157, 1967.
4. Replogle, R. L., Meiselman, J. J., and Merrill,
E. W. : Clinical implications of blood
rheol-ogy studies. Circulation, 36: 148, 1967.
5. Replogle, R. L., Kundler, H., and Cross, R. E.:
Studies on the hemodynamic importance of blood viscosity. J. Thor. Cardiovas. Surg., 50:658, 1965.
6. Jacobeus, U. : Studies on the effect of dextran on
the coagulation of the blood. Acta Med.
Scand. (Suppi. 322), 1957.
7. Cohn, J. N. : Blood pressure measurement in
shock. Mechanism of inaccuracy in
ausculta-tory and palpatory methods. J.A.M.A.,
199:118, 1967.
8. Wilson, J. N., Grow, J. B., Demong, C. V., Prevedel, A. E., and Owens, J. C. : Central
venous pressure in optimal blood volume