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Review Article
Abstract
Trauma is a leading cause of death worldwide, and almost 30% of trauma deaths are due to blood loss. A number of concerns
have been raised regarding the advisability of the classic principles of aggressive crystalloid resuscitation in traumatic hemorrhagic
shock. Some recent studies have shown that early volume restoration in certain types of trauma before definite hemostasis may
result in accelerated blood loss, hypothermia, and dilutional coagulopathy. This review discusses the advances and changes in
protocols in fluid resuscitation and blood transfusion for treatment of traumatic hemorrhage shock. The concept of low volume
fluid resuscitation also known as permissive hypotension avoids the adverse effects of early aggressive resuscitation while
maintaining a level of tissue perfusion that although lower than normal, is adequate for short periods. Permissive hypotension
is part of the damage control resuscitation strategy, which targets the conditions that exacerbate hemorrhage. The elements
of this strategy are permissive hypotension, minimization of crystalloid resuscitation, control of hypothermia, prevention of
acidosis, and early use of blood products to minimize coagulopathy.
Key words: Damage control resuscitation, fluid resuscitation, massive transfusion protocol, permissive hypotension
Introduction
Globally, injuries contribute to around 10% of total deaths
and 15% of disability-adjusted life-years.[1] Recent studies
suggest that injuries contribute to 13-18% of total deaths
in India. Road traffic injuries (RTIs) place a huge burden
on the health sector in terms of prehospital care, acute care,
and rehabilitation.[1] According to WHO, RTIs are the
sixth leading cause of deaths in India with a greater share
of hospitalizations, deaths, disabilities and socioeconomic
losses in young and middle-age populations. Most of
the deaths occur due to poor decision and inappropriate
interventions. An estimated 10-20% of these deaths are
potentially preventable with better control of bleeding.
Early hemorrhage within 6 h after incurring an injury
Address for correspondence: Dr. Veena Chatrath,
41/3, Mall Road, Amritsar - 143 001,
Punjab, India.
E-mail: drveenachatrath@yahoo.com
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DOI:
10.4103/0970-9185.161664
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Chatrath, et al.: Fluid resuscitation in trauma
Resuscitation Injury
Another parameter that needs to be understood is resuscitation
injury. In the setting of trauma, capillary permeability increases,
leading to a loss of intravascular fluid into the interstitial
space. Moreover, acidosis that results from significant trauma
impairs cardiac function.[6] Treating these patients with a
large volume of crystalloids can lead to cellular swelling and
resulting dysfunction.[6] Fluid causes dilutional coagulopathy,
clot disruption from increased blood flow, decreased blood
viscosity and interstitial edema. There is increased risk of
acute respiratory distress syndrome and multi-organ failure.
Large volume crystalloid resuscitation causes gastrointestinal
and cardiac complications,[5] increased extremity compartment
pressures [7] and coagulation disturbances. Abdominal
compartment syndrome is clearly proven to be a result of
large volume crystalloid resuscitation.[8] Secondary abdominal
compartment syndrome occurs in patients without any
underlying abdominal injury, has mortality >50% and is
clearly linked to over aggressive fluid resuscitation strategies.[8]
Pathophysiology of Hypovolemic
Micro-circulation
Hypovolemia and blood loss lead to inadequate perfusion of
micro-circulation that result in insufficient oxygen availability
to meet the needs of mitochondrial oxidative phosphorylation.
Adequate micro-circulation relies on the function of the
different components of micro-circulation. Red and white
blood cells, endothelial cells and smooth muscle cells have
to function in close harmony to ensure adequate microcirculatory blood flow to transport oxygen to the tissues. The
function of these components is affected by hypovolemia.
Administration of fluids to correct hypovolemia may modulate
micro-circulatory function by various mechanisms. The flow is
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Chatrath, et al.: Fluid resuscitation in trauma
Hemostatic resuscitation
The term denotes the very early use of blood and blood
products as primary resuscitation fluids to treat intrinsic acute
traumatic coagulopathy and to prevent the development of
dilutional coagulopathy. It is initiated within minutes of arrival
in the emergency department. First resuscitation is limited
to keep blood pressure at 90 mmHg, preventing renewed
bleeding from recently clotted vessels. Secondly, intravascular
volume restoration is accomplished using thawed plasma a
primary resuscitation fluid in at least 1:1 ratio with packed
red blood cells (PRBC). Causalities who require continued
resuscitation, massive transfusion protocol (MTP) is activated
with delivery of 6 units of plasma, 6 units of PRBCs and 10
units of cryoprecipitate. Ruskin et al.[28] showed that deaths
from trauma significantly decreased after introduction of MTP.
Massive transfusion however may cause hypocalcemia,
hyperkalemia, hypomagnesemia, acid base disturbances,
hypothermia, thrombocytopenia, and coagulopathy. Recent
studies indicate that packed red cells replacement along with fresh
frozen plasma (FFP) and platelet concentrates early in trauma
management prevents dilutional effects and markedly improves
the coagulopathic bleeding in trauma patients. The aggressive
hemostatic resuscitation should be combined with equally
aggressive control of bleeding. Tranexamic acid, an antifibrinolytic
agent, is to be given to all patients with uncontrolled bleeding
who required blood transfusion.[13] As per CRASH-2 trial[29]
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Chatrath, et al.: Fluid resuscitation in trauma
Table 1: Adapted from management of hypovolemic shock in trauma patient; NSW Institute of Trauma and Injury
Management; January 2007 SH PN: (T1) 070034
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Chatrath, et al.: Fluid resuscitation in trauma
is an indirect marker of oxygen debt, tissue hypoperfusion and the severity of hemorrhagic shock. Base
deficit gives indirect estimation of acidosis due to
impaired perfusion. Repeated lactate determinations
represent a reliable prognostic index for patients with
circulatory shock.
DCR should be employed in severely injured patient
presenting with deep hemorrhagic shocks, signs of
ongoing bleeding and coagulopathy, hypothermia,
acidosis, inaccessible major anatomical injury.
Crystalloid should be applied initially for bleeding
trauma patients (Grade IB). Hypertonic saline (HTS)
to be considered for hemodynamically unstable patients
(Grade 2B). Addition of colloid to be considered within
the prescribed limits for each solution in hemodynamically
unstable patients (Grade 2C).
Early FFP in patients with massive bleeding (Grade IB).
Platelets to be administered to maintain the count above
50 109/L (Grade IC). However, maintain the count
above 100 109/L in patients with multiple trauma
who are severely bleeding or have traumatic brain trauma
(Grade 2C).
Tranexamic acid 10-15 mg/kg followed by infusion of
1-5 mg/kg/h (Grade IB).
Target hemoglobin of 7-9 gm% (Grade IC).
Monitoring of ionized calcium during massive transfusion
(Grade IC). Calcium chloride to be administered if
ionized calcium levels are low or electrocardiographic
changes suggests hypocalcemia (Grade 2C).
Hypertonic saline
Hypertonic saline
with dextran
Blood transfusion
Advantages
Provides better buffer for metabolic
acidosis
Commonly used for resuscitation, no
immunological effects
Decreased volume required as compared
to crystalloids
Disadvantages
Increases endothelial dysfunction and neutrophil activation with
increase in cellular damage[40]
Causes hyperchloremic acidosis especially when given in large doses,
increased incidence of dilutional coagulopathy[41]
1.68 fold increase in relative risk of death as compared to crystalloids[42]
Leakage to extra vascular spaces leads to worsening of edema
Increased mortality for patients with TBI who were resuscitated with
4% albumin (SAFE trail 2007 sub group analysis)[43]
Concerns regarding hypernatremia and hyperchloremia exists[13]
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Chatrath, et al.: Fluid resuscitation in trauma
3.
4.
5.
6.
11.
Conclusion
14.
15.
7.
8.
9.
10.
12.
13.
16.
17.
18.
19.
20.
21.
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Dates
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