Fluid and Blood

Resuscitation in Traumatic
Shock
David M. Somand
Kevin R. Ward

INTRODUCTION
Circulatory shock has a high mortality. Severe hemorrhage after injury
carries a mortality rate of 30% to 40% and is responsible for almost 50% of
deaths occurring within 24 hours of injury.1,2 Septic shock has a mortality
of up to 50%.3 Resuscitation, starting in the prehospital setting and continuing
throughout the victim’s care in the ED and on into the hospital, has
the goal of restoring the necessary level of tissue perfusion and oxygenation
for survival while simultaneously limiting further volume loss.
Intravascular volume depletion is a common feature of circulatory
shock; crystalloids, colloids, and blood products (packed red blood cells

and plasma) are the primary volume expanders to reverse intravascular

volume depletion. This chapter focuses on the issues related to fluid and
blood resuscitation in traumatic shock, with an emphasis on hemorrhagic
shock. Processes that cause loss of plasma fluid and electrolytes
(e.g., dehydration, burns, sepsis), often requiring aggressive fluid therapy,
are discussed in other chapters (see chapters 150, “Toxic Shock
Syndromes,” 151, “Sepsis,” and 216, “Thermal Burns”).
The principal objectives of fluid and blood resuscitation in traumatic
shock are: (1) to restore intravascular volume sufficient to maintain oxygen-
carrying capacity and tissue perfusion for adequate cellular oxygen
delivery, and (2) to prevent or correct derangements in coagulation.
PATHOPHYSIOLOGY
Circulatory shock is a state of impaired oxidative metabolism and
homeostasis due to inadequate oxygen delivery to meet metabolic
demand, and hypoperfusion leading to inadequate cellular waste
removal. Acute shock triggers a complex range of physiologic responses
that compensate for intravascular volume loss and maintain perfusion to
the most important vascular beds. Shock also produces a global insult to
the vascular endothelium that activates the coagulation and inflammatory
systems (Figure 13-1). When uncorrected, coagulopathy, additional
inflammation, and organ system damage result.
While moderate transient hypoperfusion may be well tolerated, prolonged
or severe hypoperfusion leads to accumulation of oxygen debt
and progressive cellular and organ dysfunction. If rapid and severe, sudden
cardiovascular collapse and death may occur.
Coagulopathy observed in trauma victims, termed trauma-induced
coagulopathy, is ascribed to a combination of factors beginning with loss
of coagulation factors from hemorrhage, followed by
hemodilution from crystalloid resuscitation, and
then exacerbated by acidosis (evidenced by a base
deficit) and hypothermia that occur during the
course of ongoing hemorrhage and resuscitation.4
These same principles also apply to other causes of
shock.5 However, acidosis does not, by itself, have a
significant effect on coagulation until the pH
decreases below 7.0.6
The lethal triad of hypothermia, hemodilution,
and acidosis can be viewed a partially iatrogenic
based on the type of resuscitation provided. The
normal total circulating volume of an adult is
approximately 7% of ideal body weight or about 5 L
for an average 70-kg adult patient divided into
about 3 L of plasma and 2 L of red blood cell volume
(Table 13-1). Understanding this distribution explains
how trauma-induced coagulopathy can be iatrogenically
produced.
Factors exacerbating trauma-induced coagulopathy,
including hyperfibrinolysis and clotting factor
and platelet consumption or dysfunction, are related to the degree of injury and hemorrhage.7
Early trauma-induced coagulopathy
is characterized by anticoagulation and hyperfibrinolysis, likely
modulated through the protein C pathway. Endothelial damage associated
with trauma or sepsis stimulates an increase in thrombomodulin
expression on the endothelium that complexes with thrombin and in turn
activates protein C (Figure 13-2). Complexed thrombin is now no longer
available for its usual hemostatic role of cleaving fibrinogen to form
fibrin. Subsequent consumption of plasminogen activator inhibitor-1 by
activated protein C contributes to hyperfibrinolysis (Figure 13-2).8
Thrombomodulin normally found in the endothelium may be viewed
as protective because it is able to sequester thrombin and thus allow for
generation of adequate levels of protein C to prevent thrombosis caused
by low-flow states. However, on a mass systemic level, this appropriate
local response may become pathologic, resulting in clotting inhibition.
TABLE 13-1 Adult Fluid Spaces
Fluid Compartment % Body Weight* % Body Water* Volume* (70 kg)
Total body water 60 100 42 L
Intracellular 40 67 28 L
Extracellular 20 33 14 L
Interstitial 15 25 10 L
Intravascular ~7–8 ~11–13 ~5.0–5.5 L
Plasma ~4.0–4.5 ~7 ~3.0–3.5 L
Red blood cells† ~3.0–3.5 ~5 ~2.0–2.5 L
*Approximate percentage and amount.
†Percentages do not add up to 100% because fluid contained within intravascular red blood cells
is
included within the intracellular fluid compartment.

CLINICAL FEATURES
The clinical appearance of acute traumatic shock is variable and depends
on the cause, rate, volume, and duration of volume loss or bleeding; the
presence of other acute disorders; the effects of current medications; and
the patient’s baseline physiologic status.
The hemodynamic response to acute severe hemorrhage-induced
hypovolemia traditionally includes tachycardia, hypotension, and signs
of poor peripheral perfusion (cool, pale, clammy extremities with weak
peripheral pulses and prolonged capillary refill). Arterial and venous
vasoconstriction leads to a narrowing of the pulse pressure. Cerebral
hypoperfusion causes alterations in mental status. With increasing blood
loss, signs and symptoms become more pronounced. Classification of
hemorrhage severity as a percentage of blood volume loss based on vital
signs is not accurate and should not be used to guide ED resuscitation.9

Patients with excellent baseline physiologic status (e.g., young athletes)

may have such a robust compensatory response to hemorrhage
that they appear stable and do not manifest tachycardia or hypotension,
even with large blood volume loss. Signs of peripheral hypoperfusion
and subtle mental status alterations may be the only clues that the severity
of hemorrhage is greater than predicted based on hemodynamic
parameters. Elderly patients may not develop tachycardia due to
underlying heart disease or medications such as β-adrenergic blockers.
Bradycardia or lack of tachycardia may occur in about 30% of patients
with intra-abdominal hemorrhage from increased vagal tone in response
to hemoperitoneum. In a pregnant trauma patient, compression of the
inferior vena cava by the gravid uterus can decrease central venous
return and worsen hypotension and tachycardia in the setting of less
severe hemorrhage.

DIAGNOSIS
Vital signs offer little value unless they are in extreme low ranges.
Arterial blood pressure does not adequately reflect cardiac output or
regional perfusion. Clinical evidence of peripheral hypoperfusion is
useful but is not a quantitative measurement. Metabolic information
(discussed below), assessment of mechanisms of injury and illness,
and appropriate imaging studies offer the best chance for early recognition
of severe hemorrhage and for guiding an appropriate response
to treatment.
There is a biphasic relationship between oxygen consumption and
oxygen delivery (Figure 13-3). While this relationship exists for the body
as a whole, it also exists for each individual organ system and is largely
mediated by the microcirculation. Oxygen debt develops in tissues or
organs when oxygen delivery does not meet the metabolic demands and
represents the amount of extra oxygen that is needed to metabolize the
accumulated products of anaerobic metabolism once perfusion is
restored. Oxygen debt is the accumulation of multiple oxygen deficits
over time and is a measure of whole-body ischemia. Oxygen debt is the
only physiologic measure that has clearly been linked to both mortality
and even morbidity in the form of multiple organ failure after shock. The
degree of oxygen debt incurred after injury has also been clearly linked to
inflammation.10
Measurements of lactate and base deficit are in fairly ubiquitous use
in trauma centers and EDs and are now even being used as point-of-care
testing in the prehospital setting as a triage tool. Using lactate and/or base deficit as a
resuscitation trigger and its clearance/normalization as
an endpoint is prudent and is associated with improvements in survival.
However, elevated lactate and base deficit is a late finding, which is first
preceded by increases in oxygen extraction as indicated by a decrease in
indicators of oxygen consumption such as mixed or central venous
hemoglobin oxygen saturation (Figure 13-2). Furthermore, improvements
in oxygen delivery resulting in lactate clearance do not indicate
that oxygen extraction is normal.
Although lactate is also a measure of oxygen debt, its resolution during
resuscitation does not ensure the important repayment and resolution
of oxygen debt. Lactate also suffers from the intermittent and timedependent
nature of its measure and change. To counter these,
continuous measures of oxygen consumption surrogates are available in
the form of invasive oximetric catheters measuring central venous oxygen
saturation (Scvo2) and tissue oxygen saturation (Sto2) noninvasively
from target tissues such as skeletal muscle using near-infrared spectroscopy.
Sto2 measurements with infrared spectroscopy are based on the
fact that tissue blood volume is 70% to 80% venous blood with the
remaining 10% to 20% a combination of arterial and capillary blood.
Thus aggregate measures of hemoglobin oxygenation in the tissue are
heavily dominated by the venous blood and thus the postextraction
compartment. Although not an exact mirror of Scvo2, ensuring Sto2
values above 50% appears to be reasonable from both a diagnostic and
treatment standpoint to begin and sustain hemostatic resuscitation. A
target Sto2 or Scvo2 between 60% and 70% should be maintained to help
ensure resolution of tissue hypoxia.

TREATMENT
Resuscitation begins in the prehospital setting and continues in the
ED. The priority for prehospital care is treatment of life-threatening
conditions and rapid transport to an appropriate facility. For the hemorrhaging
patient, this entails assuring adequate ventilation and oxygenation
(including securing an airway if necessary), controlling
external bleeding (if present), and protecting the spinal cord (if potentially
vulnerable).
In the ED, restore intravascular volume to reverse or limit systemic
and regional hypoperfusion, maintain oxygen-carrying capacity so
that tissue oxygen delivery meets demand, and limit ongoing blood
loss and prevent the development of coagulopathy. From the
moment resuscitation begins, prevent the development of hypothermia
by keeping the patient warm and administering warmed IV
fluids and blood products.11 Endogenous hypothermia occurs
when heat production from cellular respiration is decreased by
hypoperfusion and inadequate tissue oxygen delivery. Major
causes of exogenous hypothermia are exposure and the use of
below-body-temperature fluid and blood resuscitation. Apply
external warming devices early to prevent external heat escape.
Warming devices that allow for the rapid warming of infused fluid
and blood should be used for all patients in whom large-volume
resuscitation is undertaken.11
 AIRWAY CONTROL, VENTILATION, AND OXYGENATION
If spontaneous ventilation is not adequate, intubate and ventilate to
achieve an arterial hemoglobin oxygen saturation of ≥94%. Identify
and treat potential respiratory conditions such as pneumothorax,
tension pneumothorax, hemothroax, or upper airway obstruction.
 VASCULAR ACCESS AND MONITORING
Establish adequate IV access concurrent with airway management.
Large-bore (14- to 16-gauge in adults) peripheral lines may be adequate
if two or more can be secured. Central venous access may be
necessary. Intraosseous lines are suitable for resuscitation.
Institute continuous ECG heart rate monitoring, continuous
pulse oximetry, and, if possible, continuous end-tidal carbon dioxide
monitoring. Monitor arterial blood pressure, mental status, and
peripheral perfusion frequently. Bedside US is useful to identify

intraperitoneal bleeding, assess cardiac function

and volume status, and assist in central venous
cannulation.12,13
 HEMOSTATIC-HYPOTENSIVE RESUSCITATION
Hemostatic resuscitation begins in the field. In
traumatic shock, the goal is deliberate hypotensive
resuscitation, so that intravascular volume
expansion is limited and blood pressure is not
normalized. Blood pressure goals are systolic
blood pressures of 80 to 90 mm Hg (10.7 to 12.0
kPa) in trauma and 90 to 95 mm Hg (12.0 to 12.7
kPa) in head injury. Normalization of blood
pressure and the raising of hydrostatic pressure
can increase hemorrhage. This is particularly
evident in noncompressible hemorrhage where raising blood pressure
could potentially “pop the clot” and reestablish active hemorrhage.
Hypotensive resuscitation targets fluid resuscitation only when systolic
blood pressure falls below 70 to 80 mm Hg (9.3 to 10.7 kPa) and/or
there is evidence of decreasing mental status and, thus cerebral hypoperfusion.
This practice has been widely adopted in combat casualty care
(see chapter 302, “Military Medicine”) and is partially supported by civilian
studies.14 Preliminary results of traumatic injury comparing low versus
traditional mean arterial pressure guided resuscitation indicate that a
lower mean arterial pressure group sustains less blood loss, requires fewer
transfusions, and has improved early and 30-day survival.15
Hypotensive resuscitation is problematic for a number of reasons,
including the inability to obtain frequent and accurate blood pressures
and, in the civilian world, its application to the elderly and those with
hypertension or cerebral vascular disease. Hypotensive resuscitation
should not be used in patients with myocardial disease, cerebral ischemia,
or traumatic brain injury. Obviously there is not an unlimited time
span that patients can tolerate hypotensive resuscitation. From a cellular
standpoint, patients will at some time incur irreversible damage from
prolonged tissue hypoxia if adequate tissue oxygenation is not restored.
 ISOTONIC CRYSTALLOID SOLUTIONS
Isotonic crystalloids, normal saline, and lactated Ringer’s solution are
the most commonly used resuscitation fluids in the United States. Concerns
about each fluid are: (1) infusion of large volumes of either normal
saline or lactated Ringer’s solution can cause increased neutrophil activation,
(2) lactated Ringer’s solution can increase cytokine release and
may increase lactic acidosis when given in large volumes, and (3) normal
saline can exacerbate intracellular potassium depletion and cause hyperchloremic
acidosis.16
Crystalloid solutions are isotonic but hypo-oncotic, because they lack
the large protein molecules present in the plasma. Low oncotic pressure
results in substantial shifts of crystalloid to the extravascular space corresponding
to the relative size of the intravascular and interstitial fluid
compartments (Table 13-2). This was the physiologic basis for the 3:1
ratio for crystalloid to blood. For every amount of blood lost, three times
that amount of isotonic crystalloid is required to restore intravascular
volume because, at best, about 30% of the infused fluid stays intravascular.
Based on this rule, a loss of 1 L of blood (about 15% to 20% of total
circulating blood volume) would require about 3 L of isotonic crystalloid
to restore normovolemia, assuming no ongoing blood loss. Bearing this
in mind, the recommendations for initial fluid resuscitation have been to
administer 2 to 3 L of crystalloid solution in acute hemorrhage and assess
the response before initiating blood transfusion. In light of the new data
reflecting improved outcomes with plasma-based resuscitation in traumatic
hemorrhage, no more than 2 L of crystalloid solution should be
administered before giving serious consideration to using blood products,
especially if ongoing hemorrhage is expected.
Common modifications of isotonic fluids include use of acetate
instead of lactate in Ringer’s solution, Hartmann’s solution, and Plasma-
Lyte (Table 13-3). Plasma-Lyte is the shared name for a family of isotonic
crystalloid solutions available worldwide, marketed with variation
in composition according to regional preferences. Solutions containing
lactate or acetate are considered balanced crystalloids because they are
buffered and have a lower chloride concentration compared to normal
saline. There is evidence of low confidence that balanced crystalloids are
associated with reduced mortality compared with normal saline when
used for fluid resuscitation in sepsis.17

 COLLOID SOLUTIONS
Colloid solutions contain larger molecular weight particles that have
oncotic pressures similar to normal plasma proteins. Therefore, colloids
theoretically have several advantages during resuscitation. They would
be expected to remain in the intravascular space, replacing plasma proteins
lost due to 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, or third-spacing,
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 eventual extravascular leakage
of these larger colloid molecules.18
The colloids used as resuscitation fluids are a heterogeneous group of
agents with widely varying characteristics and effects. These agents have
no proven consistent benefit, and there is evidence of harm in some
patients with critical illness.19,20
Hetastarch is a high-molecular-weight polysaccharide that has no
proven benefit in critically ill patients.21 Currently, for logistical reasons
of weight and size, hetastarch is the recommended fluid of choice for the
far forward resuscitation of battlefield casualties.22 It is used as a part of
a hypotensive resuscitation strategy with no more than 1000 mL to be
given. The administration of 1000 mL of hetastarch is theoretically equal
to the administration of 3 L of isotonic crystalloid.
 HYPERTONIC SOLUTIONS
Hypertonic saline (7.5% saline) has been proposed as a potential crystalloid
alternative that would limit the tissue edema effects that are
often of concern with isotonic crystalloid solutions. Hypertonic saline
has anti-inflammatory and immunomodulatory effects, with demonstrable
decrease in lung and intestinal injury in animal models of hemorrhagic
shock.18 The intravascular shift of fluid from the extravascular
space may be potentially beneficial in head trauma patients by limiting
cerebral edema, lowering intracranial pressure, and improving cerebral
perfusion. The addition of dextran to hypertonic saline was aimed at
sustaining the hemodynamic effect of the hypertonic saline. The volume
of hypertonic saline solution that can be given during resuscitation
is limited due to the potential for hypernatremia. Similar to hetastarch,
an approach using smaller volumes (250 mL) of hypertonic saline
(7.5%) has also been advocated. Randomized controlled trials have not
demonstrated a clinically significant difference in outcome when
hypertonic saline was compared with conventional isotonic fluid.23
However, these studies did not generally incorporate hypotensive resuscitation
as a part of the overall strategy, and in the prehospital trail,
transport times to trauma centers were short.24
 PACKED RED BLOOD CELLS
Packed red blood cells (PRBCs) are the most commonly transfused
blood product (see chapter 238). Using only PRBCs in the patient with
traumatic shock and ongoing bleeding (without plasma and platelets)
will do little to promote hemostasis and may not restore tissue oxygenation.
If hemorrhage is definitively controlled, do not transfuse if the
hemoglobin concentration is > 10 g/dL (> 100 g/L). Consensus recommendations
for transfusion are a hemoglobin concentration between
6 and 7 g/dL (60 to 70 g/L) for those without cardiopulmonary, cerebral,
or peripheral vascular disease.25 For a hemoglobin between 6 and
10 g/dL (60 to 100 g/L), use clinical judgement for transfusion.
When possible, typed and cross-matched blood is preferable. However,
if time and the patient’s clinical status do not permit full crossmatching,
type-specific blood is the next option, followed by low-titer
O-negative blood. In U.S. blood banks, whole blood is not stocked, and
only PRBCs are available (see the chapter 302 for further discussion of
whole-blood transfusion).
PRBC transfusion obviously restores lost hemoglobin. Using current
preservatives, PRBCs can be stored for up to 45 days, and the average age
of a unit of blood administered in the United States is about 21 days.
Stored red blood cells can lose deformability, limiting their ability to pass
normally through capillary beds or even resulting in capillary plugging.
The oxygen dissociation curve is altered by loss of 2,3-diphosphoglycerate
in the erythrocytes of stored PRBCs, impeding the off-loading of
oxygen at the tissue level.26 Despite these changes, no consistent harm
has been identified with use of “older” stored blood.27,28
 FRESH FROZEN PLASMA
Fresh frozen plasma (FFP) is plasma obtained after the separation of
whole blood from red blood cells and platelets and then frozen within
8 hours. A unit of FFP has a volume of 200 to 250 mL and contains all
the coagulation factors present in fresh blood. Kept frozen, FFP can
be stored for up to a year after the unit was collected. It takes between
15 and 20 minutes to thaw a unit of FFP in a 37°C water bath, which
can limit availability in a massive transfusion situation. However,
some major trauma centers and their respective blood banks keep
thawed FFP (kept at 1°C to 6°C) available for immediate use. FFP may
be kept thawed at this temperature for up to 5 days with little degradation
of plasma proteins. FFP ABO compatibility is required, but
because there are no red cells in FFP, Rh compatibility is less important,
and universal donor FFP is typically AB+ (see chapter 238,
“Transfusion Therapy”).
 PLATELETS
Platelets are collected from whole-blood donations or from single
donors using apheresis techniques and can only be stored for up to 5 days.
Six units of pooled random-donor platelet concentrate or one apheresiscollected
single-donor platelet concentrate in an adult will increase
platelet count up to 50,000/mm3 (50 . 109/L).
 MASSIVE TRANSFUSION PROTOCOLS
Massive transfusion is generally defined as the requirement for >10
units of PRBCs within the first 24 hours of injury. Massive transfusion
is not a substitute for definitive surgical hemostasis but enhances the
ability to achieve surgical hemostasis and to limit complications.29,30
Draw sufficient specimens from the patient early in anticipated massive
transfusion because once the patient has received close to one
blood volume of transfused products, new blood specimens will contain
so much donor blood that cross-matching of subsequent units is
difficult. Initially use isotonic solutions to begin resuscitation in predetermined
aliquots (250 to 500 mL) while assessing the likelihood of
ongoing active hemorrhage and the need for, type, and timing of
hemostasis and for hypotensive resuscitation.31,32 Variables predictive
of need for massive transfusion include penetrating mechanism of
injury, positive FAST examination, blood pressure <90 mm Hg (< 12.0
kPa), and pulse rate >120 beats/min.33,34 If hemorrhage is clinically
significant and immediate hemostasis is not achievable, transition
from crystalloid-based resuscitation to a plasma-based massive transfusion
protocol.
An estimated 10% of military trauma patients and 3% to 5% of civilian
trauma patients receive massive transfusion.1 Soldiers receiving high ratios
of plasma to PRBC (a plasma:PRBC ratio of about 1:1.4) have significantly
improved survival rates than those receiving lower ratios (between 1:1.8
and 1:2.5). Additional evidence supporting this also comes from combat
casualty care data suggesting that early administration of fresh whole
blood (something not currently practical in civilian trauma) offers survival
advantages.18,35 These survival observations using high plasma-to-
PRBC ratios were confirmed by civilian studies, which also appear to
indicate less incidence of trauma-induced coagulopathy.33,36
High plasma-to-PRBC ratio resuscitation appears to also offer survival
benefit independent of coagulopathy, and plasma may enhance cell
survival by endothelial repair and reducing vascular permeability. It may
also be that plasma is simply a superior fluid for perfusion and tissue
oxygenation restoration. In addition, many trauma centers now include
early platelet administration in predetermined ratios to plasma and
PRBC in their resuscitation protocols based on findings that platelet
function can rapidly decrease soon after trauma.1,34
Studies routinely using FFP and platelets with PRBCs during massive
transfusion have yielded mixed results on reducing mortality.34,37 The best
ratio of PRBCs to platelets to FFP during massive transfusion is controversial.
38 Some experts advocate a 1:1:1 ratio, although lower ratios of
platelets and FFP have been used without evidence of inferiority.39 Likewise,
the benefits with adjunctive agents such as calcium chloride, prothrombin
complex concentrates, and fibrinogen concentrate included in
some protocols are unknown. Tranexamic acid (an antifibrinolytic) is
advocated early in the resuscitation process of major trauma victims
based on the early fibrinolytic phase of trauma-induced coagulopathy
and on clinical studies suggesting improved survival.40 An institutionspecific
massive transfusion protocol is recommended to guide the clinician
when ordering blood components and to facilitate release from the
blood bank (Figure 13-4). Tranexamic acid, an antifibrinolytic agent, is
not currently a component of massive transfusion protocols in the United
States. Its use is discussed in the chapters 254, “Trauma in Adults” and
302, “Military Medicine.” If given, it must be administered as soon as possible
and within 3 hours of injury. The dose is 1 gram IV bolus in 100 mL
normal saline.
Calcium PRBCs and FFP contain citrate that can complex calcium,
producing life-threatening hypocalcemia.41 Most massive transfusion
protocols include the administration of calcium and monitoring of ionized
calcium. Calcium chloride is preferred over calcium gluconate
because a well-perfused liver is required to liberate more free calcium
from calcium gluconate. Maintain ionized calcium levels at or above
0.9 mmol/L.42
Thromboelastography and Thromboelastometry The blood
coagulation system consists of nearly 80 very tightly coupled biochemical
reactions. Conventional coagulation testing such as the prothrombin
time and activated partial thromboplastin time do not take
into account the cellular components of the clot such as red cells and
platelets. Because the blood clot itself consists of a complex threedimensional
network of cross-linked fibers made of fibrin, platelets,
and red cells entrapped within this mesh, newer viscoelastic tests such
as thromboelastography or thromboelastometry are being developed
to measure the physical and dynamic characteristics of clotting.
Thromboelastography and thromboelastometry can detect traumainduced
coagulopathy and can be used to guide massive transfusion
protocols better than traditional prothrombin time and activated partial
thromboplastin time assays.43 However, impact on clinical care is
uncertain at this time.43

COMPLICATIONS
 TRANSFUSION-RELATED ACUTE LUNG INJURY
Acute lung injury is the leading cause of transfusion-related fatalities. It
develops within 6 hours of blood transfusion and is felt to be related to
an inflammatory reaction.44 Care is supportive.
 TRANSFUSION-ASSOCIATED CIRCULATORY OVERLOAD
Circulatory overload occurs when the recipient’s circulatory system is
overwhelmed by the rate of transfusion or the volume of products transfused.
45 Clinically, it is characterized by the acute onset of dyspnea,
hypertension, tachypnea and tachycardia, and marked elevation in brain
natriuretic peptide levels. Care often involves rapid diuresis.
REFERENCES
The complete reference list is available online at www.TintinalliEM.com.