Introduction
Shock is a state at which the cardiovascular system failure occurs that causes tissue
perfusion disorder. This condition causes hypoxia,
cellular metabolism disorders, tissue damage, organ failure and death.
Pathophysiology of hemorrhagic shock is a
shortage of intravascular volume that causes a
decrease in venous return resulting in decreased ventricular filling, decrease
in stroke volume and cardiac output, resulting in tissue perfusion disorder.
Resuscitation on hemorrhagic shock would
reduce mortality. Management of hemorrhagic shock is intended to restore the
circulating volume, tissue perfusion by correcting hemodynamics,
control bleeding, stabilize the circulation volume, optimization of oxygen
transport and if necessary giving vasoconstrictor when blood pressure remains
low after the administration of fluid loading. Giving fluids are important in
the management of hemorrhagic shock starting with crystalloid /
colloid followed by transfusion of blood components.
Coagulopathy associated with
massive transfusion remains a significant clinical problem. Strategic therapy
include maintaining tissue perfusion, correction of hypothermia and anemia, and the use of hemostatic products to correct
microvascular bleeding.
STAGES OF SHOCK
Shock has several stages before it becomes decompensated
or irreversible condition, as described in the following figures:
STAGE 1 ANTICIPATION STAGE
The disease has started but remains local
Parameters
are stable and within normal limits. There is usually enough time to diagnose
and treat the underlying condition.
STAGE
2. PRE-SHOCK SLIDE
The disease is now
systemic.Parameters drift, slip and slide... and start hugging the upper or
lower limit of their normal range.
STAGE 3 COMPENSATED SHOCK
Compensated shock can start with low normal blood pressure: a condition
called "normotensive, cryptic
shock". Many physicians fail to
recognize the early part of this stage. Recognition of compensated shock is particularly important in patient
with DHF. Clinicans should be alert on
the following signs: Capillary refill time > 2 seconds; narrowing of pulse
pressure, tachycardia, tachypneoa and cold extremities.
STAGE
4 DECOMPENSATED
SHOCK, REVERSIBLE
Now everybody call this "SHOCK"
because hypotension is always present at this stage., Normotension can only be
restored with intravenous fluid (if indicated) and/or vasopressors
STAGE 5 DECOMPENSATED IRREVERSIBLE
SHOCK
Microvascular and organ damage are now
irreversible (untreatable)
CLASSIFICATION OF SHOCK
The degree of hemorrhagic shock can be roughly estimated according to
several clinical parameters, but a lot is determined by the response to fluid
resuscitation 1.
Class 1
|
Class 2
|
Class 3
|
Class 4
|
|
Amount of
Blood loss(ml)/%
|
Up to 750
Up to 15%
|
1000-1250
20-25%
|
1500-1800
30-35%
|
2000-2500
>40%
|
HR
|
72-84
|
>110
|
>120
|
>140
|
BP
|
118/72
|
110/80
|
70-90/50-
60
|
Sys < 50-
60
|
Resp
rate
|
14-20
|
20-30
|
30-40
|
>35
|
Urine output/hr
|
30-35 ml
|
25-30 ml
|
5-15
ml
|
-
|
CNS
|
Slightly
anxious
|
Anxious
|
Anxious
&
confused
|
Confused
,lethargy
|
Lactic acid
|
Normal
|
Transition
|
Increased
|
increased
|
Management
Initial therapy in the setting of acute hemorrhage should involve
securing the airway, assuring adequate ventilation and oxygenation, controlling
external bleeding (if present), and protecting the spinal cord (if potentially
vulnerable). Fluid resuscitation should be determined with the following
objectives in mind: (1) restoring intravascular volume sufficiently to reverse
systemic hypoperfusion and limit regional hypoperfusion; (2) maintaining
adequate oxygen-carrying capacity so that tissue oxygen delivery meets critical
tissue oxygen demand; and (3) limiting ongoing loss of circulating RBCs.
Unfortunately, there are no readily available precise parameters that allow the
clinician to optimally balance these three objectives in the midst of the
dynamic physiologic changes seen in acute hemorrhage and resuscitation.
Nonetheless, the patient will most likely benefit from the clinician's best
efforts to maintain this balance until surgical control of ongoing hemorrhage
can be achieved.
Fluid Resuscitation
Intravascular volume
replacement to treat hemorrhage has been the accepted dogma for decades. The
goal of restoring normal intravascular volume and normal arterial blood
pressure was generally accepted for most of this time. The major area of
controversy was the optimal resuscitation fluid. However, over the past decade
the accepted practice of resuscitating patients to a normal blood pressure has
been questioned. The early studies that supported aggressive volume replacement
were performed in laboratory models of controlled hemorrhage. In such a
circumstance, rapidly restoring normovolemia optimized outcome and had no
appreciable adverse effects. 2
However, this laboratory model does not accurately reflect the clinical
situation. Most hemorrhagic shock patients have not had control of their
bleeding achieved prior to initiation of fluid resuscitation. This fact raised
concern that fluid resuscitation to a normal blood pressure might actually be
deleterious by exacerbating ongoing hemorrhage and ultimately worsening
outcome. Formation of clots at areas of vascular injury is facilitated by the
lower blood pressure that results during hemorrhage. Increased blood pressure
may dislodge these fragile developing clots. Because crystalloid solutions have
essentially no oxygen-carrying capacity, any exacerbation of hemorrhage
resulting from their infusion will lower the oxygen-carrying capacity of the
circulating blood. Laboratory models of acute vascular injury with uncontrolled
hemorrhage verified that raising the arterial blood pressure to the normal
range increased the rate of ongoing bleeding. This led to the concept of
limited volume or "hypotensive" resuscitation..3
The
goal of this limited approach is to provide sufficient fluid resuscitation to
maintain vital organ perfusion and avoid cardiovascular collapse while keeping
the arterial blood pressure relatively low (e.g., mean arterial pressure of 60
mm Hg) in the hope of limiting further loss of red blood cells until surgical
control of bleeding can be achieved. The potential adverse effect of this
approach is that it accepts the presence of regional hypoperfusion, the effects
of which are dependent on both the severity and duration of the hypoperfusion.
Splanchnic hypoperfusion is especially of concern because this may be a major
contributor to the development of subsequent multiple organ dysfunction.1
Unfortunately, accurate clinical assessment of regional hypoperfusion is not
presently possible. Thus, the optimal resuscitation end point is not clear and
likely varies with the individual patient. A randomized clinical study that
aimed to evaluate hypotensive resuscitation to a systolic blood pressure of 70
mm Hg did not show any mortality benefit for this approach. However, the target pressure of 70 mm Hg was
difficult to maintain, with the systolic blood pressure in the hypotensive
group reaching an average of 100 mm Hg. This demonstrates the difficulty of achieving
and maintaining a specific hypotensive blood pressure target in the dynamic
setting of hemorrhagic shock resuscitation. At present, this is still a concept
that has not been clearly shown to improve survival. However, it seems
reasonable to keep this concept in mind and to avoid excessive fluid
resuscitation.
Blood Transfusion
There are no clearly defined parameters that
trigger the switch from crystalloid to blood resuscitation. However, it is
generally accepted that a patient in shock that demonstrates minimal or only
modest hemodynamic improvement after rapid infusion of 2 to 3 L of crystalloid
is in need of blood transfusion. However, it would be acceptable to start blood
immediately if it is clear that the patient has suffered profound blood loss and
is on the verge of cardiovascular collapse. Some patients may have an adequate
hemodynamic response to initial crystalloid therapy that is transient. In such
cases, continued crystalloid infusion beyond the first 2 to 3 L might be used
for hemodynamic support so long as attention is paid to progressive
hemodilution and its effect on tissue oxygen delivery. This hemodilution also
lowers the concentration of clotting factors and platelets needed for intrinsic
hemostasis at bleeding sites. Serial assessment of blood hemoglobin
concentration is useful in such a situation. An American Society of
Anesthesiologists task force review found that a blood hemoglobin concentration
>10 g/dL (hematocrit >30 percent) very seldom requires blood transfusion,
whereas a level <6 g/dL (hematocrit <18 percent) almost always requires
blood transfusion. This leaves a rather wide intermediate range of
hemoglobin—between 6 and10 g/dL—where the decision to administer blood is
significantly influenced by other factors, such as the presence of underlying
disease processes that are sensitive to decreased tissue oxygen delivery and
the rate of continued blood loss, if present. Understandably, as the hemoglobin
concentration decreases, especially to 8 g/dL or less, the likelihood of needing
blood markedly increases.
When possible, typed and cross-matched blood is
preferable. However, in the acute setting where time does not permit full
cross-matching, type-specific blood is the next best option followed by
low-titer O-negative blood. Blood can be administered as whole blood or packed
RBC preparations. In U.S. blood banks, whole blood is not stocked, and only
packed RBCs are available. In the setting of massive hemorrhage with large
volumes of crystalloid and blood resuscitation, fresh-frozen plasma and
platelet transfusions may be needed to reverse the associated dilutional
coagulopathy.
Red blood cell transfusion obviously restores
lost hemoglobin, but stored blood components may also not be fully functional
and can have adverse effects, which appear to be exacerbated with longer
storage time.8 Using current preservatives, RBCs can be stored for up to 42
days and it has been reported that the average age of a unit of blood
administered in the United States is approximately 21 days old. Stored RBCs can
lose deformability, which can limit their ability to pass normally through
capillary beds, or can cause capillary plugging. The oxygen dissociation curve
is altered by loss of 2,3-diphosphoglycerate in the erythrocyte, which
adversely affects the off-loading of oxygen at the tissue level. Clinical
studies report worsening of splanchnic ischemia and an increased incidence of
multiple-organ dysfunction associated with transfusion of RBCs that have been
stored for longer than 2 weeks. Therefore, RBC transfusion, although a critical
intervention in severe hemorrhagic shock,
Transfusion of packed red blood cells and other
blood products is essential in the treatment of patients in hemorrhagic shock.
Current recommendations in stable ICU patients aim for a target hemoglobin of 7
to 9 g/dL;5 however, no prospective randomized trials have compared
restrictive and liberal transfusion regimens in trauma patients with
hemorrhagic shock. Fresh frozen plasma (FFP) should also be transfused in
patients with massive bleeding or bleeding with increases in prothrombin or
activated partial thromboplastin times 1.5 times greater than control. Civilian
trauma data show that severity of coagulopathy early after ICU admission is
predictive of mortality . Evolving data suggest more liberal transfusion of FFP
in bleeding patients, but the clinical efficacy of FFP requires further
investigation. Recent data collected from a U.S. Army combat support hospital
in patients that received massive transfusion of packed red blood cells (>10
units in 24 hours) suggests that a high plasma to RBC ratio (1:1.4 units) was
independently associated with improved survival. Platelets should be transfused
in the bleeding patient to maintain counts above 50 x 109/L. There is a
potential role for other blood products, such as fibrinogen concentrate of
cryoprecipitate, if bleeding is accompanied by a drop in fibrinogen levels to
less than 1 g/L. Pharmacologic agents such as recombinant activated coagulation
factor 7, and antifibrinolytic agents such as -aminocaproic acid, tranexamic
acid (both are synthetic lysine analogues that are competitive inhibitors of
plasmin and plasminogen), and aprotinin (protease inhibitor) may all have
potential benefits in severe hemorrhage but require further investigation.
Colloid
Resuscitation
Several colloid agents have been studied
experimentally and used clinically for the treatment of hemorrhagic shock.
Colloids have larger molecular weight particles with plasma oncotic pressures
similar to normal plasma proteins. Therefore, colloids would be expected to
remain in the intravascular space, replacing plasma proteins lost as a
consequence of hemorrhage, and more effectively restore circulating blood
volume than crystalloid solutions. An argument favoring the use of colloids has
been the concern that extravascular shift of infused crystalloid solutions has
potential adverse effects, including pulmonary interstitial edema with impaired
oxygen diffusion and intraabdominal edema with diminished bowel perfusion.
However, pathologic conditions, such as hemorrhagic shock and sepsis, lead to
increased vascular permeability that can allow for extravascular leakage of
these larger colloid molecules.
Colloid vs Crystalloid
controversies : Some additional information
The choice of colloids vs crystalloids for volume
resuscitation has long been a subject of debate among critical care
practitioners, primarily because there are data to support arguments for both
forms of therapy. In 1998, the British Medical Journal published a meta-analysis
on the use of albumin in the critically ill patient; 30 randomized, controlled
trials (RCTs) involving 1419 patients were analyzed. The conclusion was that
albumin may actually increase mortality, noted Timothy Evans, MD This review
had an impact on practice, influencing clinicians to use less albumin, but was
later criticized as being flawed when subsequent reviews did not substantiate
the authors' conclusion6. Recently, the
completion of the Saline vs Albumin Fluid Evaluation (SAFE) study has shed new
light on this issue
With the availability of various colloids with different
physochemical properties, controversy of colloid versus colloid has became
additional issue.7
Summarized below are advantages and disadvantages of both
colloids and crystalloids
Colloids
Advantages
|
Disadvantages
|
1. Plasma volume expansion
without concomitant ISF expansion
|
1. Anaphylaxis
|
2. Greater intravasculer volume
expansion for a given volume
|
2. Expensive
|
3. Longer duration of action
|
3. Albumin can aggravate myocardial
depression in shock patient, owing to albumin binding to Ca++,
which in turn decreases ionic calcium
|
4. Better tissue oxygenation
|
4. Possible coagulopathy,
impaired cross matching
|
5. Less alveolar-arterial O2
gradient
|
Crystalloids
Advantages
|
Disadvantages
|
1. Easily available
|
1. Weaker and shorter volume
effect compared to colloid
|
2. Composition resembling
plasma (acetated ringer, lactated ringer)
|
2. decreased tissue
oxygenation, owing to increased distance between microcirculation and tissue
|
3. Easy storage at room
temperature
|
|
4. Free of anaphylactic
reaction
|
|
5. Economical
|
Although interstitial edema is a more potential complication
after crystalloid resuscitation, UP TO NOW, there are no physiological,
clinical and radiological evidence that colloid is better than crystalloid in
term of pulmonary edema..
The SAFE Study
In a recent meta-analysis, an
overall excess mortality of 6% was observed in patients who were treated with
albumin. These findings generated considerable discussion and controversy,
which led to the design and implementation of the SAFE study, presented by
Simon Finfer, MD.7 This double-blind RCT enrolled 7000 patients from
16 ICUs in Australia and New Zealand over an 18-month period. Patients were
randomized to receive either 4% human albumin or normal saline from time of
admission to the ICU until death or discharge. In the first 4 days, the ratio
of albumin to saline was 1:1.4, meaning that the volumes (colloids vs
crystalloids) were not significantly different, contrary to what was expected.
Notably, there was no difference between the 2 groups in 28-day all-cause
mortality. Mean arterial blood pressure, central venous pressure, heart rate,
and incidence of new organ failure were also similar in both groups.
In a subgroup analysis,
differences between trauma and sepsis patients were observed. The relative risk
(RR) of death in patients with severe sepsis who received albumin vs saline was
0.87. The RR of death in albumin-treated patients without severe sepsis was 1.05
(P = .059). The results were the opposite in trauma patients. The overall
mortality rate in trauma patients was higher when albumin vs saline was used
for volume resuscitation (13.5% vs 10%, P = .055). When patients with traumatic
brain injury (TBI) were studied separately, the mortality rate was 24.6% in
patients who were treated with albumin compared with 15% in patients who were
treated with saline (RR 1.62, 95% confidence interval, -1.12 to 2.34, P =.009).
Furthermore, when TBI patients were excluded, there were no differences in
mortality rates among trauma patients.
Based on these results, the
administration of albumin appears to be safe for up to 28 days in a
heterogeneous population of critically ill patients, and may be beneficial in
patients with severe sepsis. However, the safety of albumin administration has
not been established in patients with traumatic injury, including TBI. Although
the differences in mortality rates in trauma and TBI patients were observed in
a subgroup analysis and consequently have limited validity, this is a strong
signal, especially in TBI patients. A new study, SAFE Brains, has been designed
to examine these differences
What are the goals of resuscitation
fluid therapy (resuscitation endpoints)?
The success criteria of
management of hemorrhagic shock, or particularly fluid resuscitation therapy
can be assessed from the following
parameters:
•
Capilary refill time <
2 sconds
•
MAP 65-70 mmHg
•
O2 sat >95%
•
Urine output >0.5 ml/kg/hour
(adults) ; > 1 ml/kg/hour (children)
•
Shock index =
HR/SBP (normal 0.5-0.7)
•
CVP 8 to12 mm Hg
•
ScvO2 > 70%
CONCLUSION
Resuscitation fluid therapy in patients with hemorrhagic shock should receive more serious attention to
reduce mortality and morbidity. The things to put into consideration are:
1.Understand the stages of hypovolemic shock
and associated pathophysiological changes
2.Early detection of compensated shock so that fluid can be given adequately
3.Know how much fluid crystalloid / colloid must
be given
4.Indication of blood transfusion
5. How to know the success of resuscitation.
References:
1. Demling RH,
Wilson RF.: Decision Making in Surgical Critical Care.B.C. Decker Inc, 1988. p
64.
2. Tintinalli JE. Tintinalls’s Emergency Medicine: A
comprehensive Study Guide, 6th e4dition
3. Stern SA:
Low-volume fluid resuscitation for presumed hemorrhagic shock: Helpful or
harmful? Curr Opin Crit Care 7:422, 2001.
4. Dutton RP, Mackenzie CF, Scalea TM: Hypotensive
resuscitation during active hemorrhage: Impact on in-hospital mortality. J
Trauma 52:1141, 2002.
5. Brunicardi, FC.
Et al. Schwartz's Principles of Surgery, 9e
6. Liolios A. Volume Resuscitation: The Crystalloid vs
Colloid Debate Revisited. Medscape 2004
7. SAFE Study Investigators: A comparison of albumin and
saline for fluid resuscitation in the intensive care unit. N Engl J Med 2004,
350:2247-2256
