Resusitation in Trauma

8/3/2019 Resusitation in Trauma

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ITACCSCURRENT PRACTICE GUIDELINES FOR

RESUSCITATION OF HAEMORRHAGIC

TRAUMA PATIENT

Dr. Sanghamitramishra

Asso. Prof

Dept. of Anaesthesiology and Critical Care


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Traumatic injury remains the leading cause of potentiallypreventable death under the age of fourty.

In addition, 50 million people globally are estimated to beinjured ordisabled every year.

Although only a minority of patients present with haemodynamicinstability, these patients have a significant chance of dying

The cause of instability must be recognized and corrected quicklyby using a systematic approach


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Once the clinician has made the diagnosis of acute blood loss,several

issues become important.

Traditional dogma suggests thatrestoration of forward flow by crystalloid

resuscitation followed by blood is optimal therapy. However, increases in blood

pressure produced by fluid may, in fact, increase blood loss by displacing the

hemostatic clot that was formed at the time of hypotension.

However, there are now data to suggest that sustained hypotension

produces a more injurious shock insult than do multiple episodes of

shock and resuscitation. Thus, the clinician must estimate the

degree of hemorrhage, the depth of shock, and the time to definitive

hemostasis when making a decision.


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Approximately 12 to 16 hours following

resuscitation, the relationship changes between

base deficit and anion gap versus serum lactate,and anion gap and base deficit no longer correlatewith lactate.

During this time, one must directly measureserum lactate as it cannot be inferred from either ofthe other two measurements.

When resuscitation decisions are based onthese parameters, therapy will be inappropriatealmost 50% of the time.


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Clearly, achieving hemostasis is the most important part ofresuscitating the trauma victim. Resuscitation efforts will

not besuccessful until blood loss is arrested.

Regardless of the resuscitation decision, patients whodemonstrate ongoing bleeding require definitive hemostasis.

Serial blood gas determinations and/or central venousoxygen saturation determination may be very helpful indetermining whether blood loss is continuing.


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Hypoperfusion is a common complication after injury.Early recognition of bleeding is key to the optimal care

of trauma patients.Normally vital signs underestimate the degree of

physiologic deficit.Limited crystalloid resuscitation is prudent initially, at

least until blood loss is controlled.New technology may soon be available to help with the

diagnosis of hemorrhage.Early use of fresh-frozen plasma is probably wise in

patients with severe hemorrhage using blood and plasma ina 1:1 ratio.

The use of factor VIIa requires further work before itsrole is clearly elucidated. It can be lifesaving in selectedpatients.


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Learning Objectives:

1) To learn the definition of shockand the common subtypes.

2) To understand the clinicaldiagnosis and progression of shock.

3) To learn the pathophysiology of shockat the cellular, tissue, organ, andwhole body level


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Shock is the systemic disease that results

from any process that impairs the systemic

delivery of oxygen to the cells of the body, orthat prevents its normal uptake and utilization.

Hemorrhage with decreased cardiac outputis the most common cause of shock intrauma patients, although it is not unusual forshock to result from a combination of events.


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Causes of Shock in the Trauma Patient

Cause Pathophysiology

Lost airway or Inability of oxygen to reach

pulmonary injury the circulation

Tension pneumothorax Diminished blood return tothe heart

Cardiac tamponade Diminished blood return to the heart

Hemorrhage Inadequate oxygen carrying capacityInadequate intravascular volume

Cardiac injury Inadequate pump function

Spinal cord injury Inappropriate vasodilatation

Inadequate pump function

Poisoning Direct failure of cellular metabolismInappropriate vasodilatation

Sepsis Direct failure of cellular metabolismInappropriate vasodilatation


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Stages and outcomes from traumatic shock. Curve A represents

compensated shock. Curve B is acute decompensated shock. Oncedecompensation has occurred, three outcomes are possible: Curve Crepresents subacute reversible shock (the patient survives). Curve D issubacute irreversible shock (the patient dies of multiple organ systemfailure). Curve E is acute irreversible shock (the patient dies ofhemorrhage and cardiovascular collapse).

O

xygendelivery/

D

emand


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After establishing a secure airway andensuring adequate oxygenation and ventilation,

the highest priority in the management of theinjured patient is to control hemorrhage.Because patients may bleed from multiple sitessimultaneously, it is imperative that a strategybe devised to identify and control all possiblesources of hemorrhage.

The control of hemorrhage is amultidisciplinary endeavor involving traumasurgeons, orthopaedic surgeons, radiologists,and anesthesiolo ists.


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Blood Loss in Trauma

Site Potential volume

External (roadway or floor) Exsanguination possible

Thorax Greater than 1.5 L per

hemithorax

Peritoneal cavity Exsanguination possible

Pelvis and retroperitoneum Exsanguination possible

Long bone fractures Tibia/Humerus, 750 mL;

Femur, 1,500 mL


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General Management of the Bleeding Patient

There must be a rapid and thorough search of the five possible

locations for blood loss following injury.

The clinical pathophysiology of hemorrhage is made manifest bytachycardia,hypotension, oliguria, and decreased mental status.

Aggressive means must be taken to stop blood loss and reversehypotension in order to prevent acidosis,coagulopathy,& hypothermia.Increasing depth and duration of hypotension has been shown to besignificantly associated with mortality.

Worsening base deficit results in statistically greater transfusion volumes,coagulopathy, and organ dysfunction. Clot formation time in healthy volunteersis significantly impaired by acidosis and the effects are reversed by buffering.Hypothermia also prolongs clotting times and causes platelet dysfunction.


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Coagulation factors are lost from circulation, consumed bycoagulation, and exhibit reduced activity because of hypothermia,acidosis, and dilution with asanguinous fluid.

Prophylactic administration of fresh-frozen plasma (FFP) orplatelets in the absence of clinical bleeding is notwarranted.However, there is a growing emphasis on the need for

earlier use of FFP before coagulation factors decline to criticallevels in patients with significant bleeding.

With ongoing bleeding in severe trauma, FFP and packed redblood cells (PRBCs) should be administered in a1:1 ratio. It iseasy to get behind in this process, because it takes 20 to 30minutes for FFP to thaw before administration.

The platelet count should be kept at a minimum of 50,000 per

Microliter.


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At laparotomy (or any operation following injury) it is absolutely necessary tocontrol hemorrhage in the most rapid fashion possible.

After hemorrhage is controlled, gastrointestinal contamination is nextaddressed.

The bloody vicious cycle (coagulopathy, hypothermia, and metabolic acidosis)should compel the trauma team to use adamage control approach.

The primary objectives of damage control are to arrest bleeding, limit

gastrointestinal contamination, and enclose the abdomen to protect viscera and limitprotein loss.

Subsequent operations are required to remove laparotomy sponges used fortamponade, restore gastrointestinal continuity if required, and to attempt abdominalwall closure when the patients condition is more acceptable.

Damage control orthopaedics, using external fixation, reduces operative timeand blood loss, and does not hinder definitive osteosynthesis conversion.


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Operating Room Priorities for the InjuredPatient

1. Control of hemorrhage2. Stop gastrointestinal contamination3. Replace coagulation factors

4. Maintain normothermia and acid-base balance5. Thorough exploration of abdomen (or other siteof injury) if condition permits6. Temporary abdominal closure if there is

significant visceral edema7. Timely transfer to intensive care unit forcontinued resuscitation8. Subsequent operations if required


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Proposed Indications for rFVIIa following Injury

Uncontrolled bleeding despite surgical or radiologic control of

large-vessel hemorrhageCoagulopathy from exsanguinating hemorrhage and failure ofconventional medical hemostatic therapySignificant red blood cell or blood component transfusion

requirementSuccess of transfusion and medical hemostatic therapyunlikely to be timely enough to ensure survivalReasonable hope for meaningful survival if coagulopathyreversedUse in remote surgical locations where traditional therapy(platelets, fresh-frozen plasma, cryoprecipitate, rewarming) fortraumatic coagulopathy is not available


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Conditions that Compromise rFVIIa Activity

Revised trauma score


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Safe principles for care of the patient with a tourniquetshould include

(1) used for the shortest time possible and removed at thefirst available opportunity,

(2) should be deflated for 10 minutes every 2 hours,

(3) use wide cuffs to allow for lower occlusion pressure,

(4) record the time when applied,

(5) Communicate tourniquet use to others down the line in the careprocess,

(6)should be removed by medical personnel only if bleeding can bemanaged and resuscitation carried out


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Hemorrhage control is a multidisciplinaryendeavor.

Lacerated organs and blood vessels must be resected orrepaired before the sequelae of hemorrhage ensue.

Medical therapy using blood products, rFVIIa, topical

hemostatic agents, or advanced hemostatic dressings mayalso be required to help restore, or compensate for, a depletedcoagulation system.

Numerous methods for hemorrhage control exist, but eachmodality must be applied to the appropriate situation.

Communication between the surgeon and anesthesiologistmust be of the highest quality, so that appropriate corrective

actions may be undertaken to preserve life.


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Various Drugs Agents That Have Some Efficacyto Reduce Bleeding and/or Transfusion Burden

Generic Name Pharmacologic ClassAprotinin Natural serine protease inhibitor

Nafamostat mesylate Synthetic serine proteaseinhibitor

e-Aminocaproic acid Lysine analogue

Tranexamic acid Lysine analogue

Desmopressin Analogue of arginine vasopressin

Recombinant Clotting factor and thrombinactivated factor VII generator

Hemostatic Drugs in Trauma andOrthopaedic Practice


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Hemostatic drugs are useful in excessive generalizedbleeding due to hyperfibrinolysis, mild hemostatic

defects, or in those patients refusing blood products.

The appropriate drug is most effective when given asprophylaxis and when adequate doses are given so

that they are not lost with the hemorrhage.

Results of ongoing trials of hemostatic drugs inorthopaedic surgery and trauma are awaited to betterdetermine their optimal uses, doses, timing of

administration, and safety.


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Fluid and Blood Therapyin Trauma

Initial evaluation of an acutely volume-depleted traumapatient will include a primary and secondary survey according to AdvancedTrauma Life Support protocol,an estimate of blood volume deficit rate of the ongoing blood loss, and

an evaluation of cardiopulmonary reserve and coexisting hepatic or renaldysfunction.

The major goal in resuscitationis tostop the bleeding,

replete intravascular volume, and restore tissue oxygenation.

Perfusion pressure and oxygenated blood flow to vitalorgans are important determinants of outcome.


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Management priorities in an acutely bleeding trauma patientinclude ventilation and oxygenation, assessment of perfusion,

estimation of volume-replacement requirements, establishment orverification of adequate intravenous access, measurement of bloodpressure, placement of electrocardiogram (ECG), pulse oximeter andcapnograph, and laboratory studies.

Placement of arterial line and close monitoring of systolic pressurevariability, temperature, urine output, arterial blood gases, hemoglobin,hematocrit, electrolytes, and parameters of coagulation is routine inseverely injuredmechanically ventilated patients.

Consideration is given to use of additional monitors (e.g., central venouscatheter, pulmonary artery catheter, transesophageal echocardiography)and provision of anesthesia as needed.


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Estimation of Blood VolumeDeficit in Trauma Patients

Site Volume (mL)

Unilateral hemothorax 3,000

Hemoperitoneum with abdominal distention 2,0005,000

Full-thickness soft tissue defect, 5 cm 3 500

Pelvic fracture 1,5002,000

Femur fracture 8001,200

Tibia fracture 350650

Smaller fracture sites 100500


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Timing and Aggressiveness ofFluid Resuscitation

Early aggressive fluid resuscitation aimed at restoration of normalhaemodynamicsl eads to increased duration and volume ofbleeding and decreased survival.

The proposed mechanisms include dilution of clotting factors,decreased blood viscosity, and blow-out of hemostatic plugs withincreasing blood pressure .

Hypotensive resuscitation, where the rate of fluid infusion iscarefully titrated to a predetermined level of lower-than-normal

blood pressure, has been advocated in patients who are notpregnant and do not have traumatic head injury.


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Consequently, in uncontrolled hemorrhagic shock,resuscitation is aimed at restoration of radial arterypulse, restoration of mental function, and systolic

blood pressure of 80 mm Hg, until the bleeding issurgically controlled.

Higher blood pressures (systolic blood pressure>100 mm Hg, mean arterial pressure >70 mm Hg)

are generally sought in head-injured and inpregnant patients.

This approach provides satisfactory resuscitation of

the trauma patient until surgical control of bleedingis achieved.


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Disadvantages of Immediate Fluid

ResuscitationDecreased blood viscosity

Blow-out of hemostatic plug

Dilution of coagulation factors

Increased blood loss

Delayed transport to definitive care

Asanguinous Fluid Options for Trauma


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Asanguinous Fluid Options for Trauma.

Lactated Ringers (LR) Preferred isotonic crystalloid solution for most trauma resuscitations. Do not mixwith blood or use in blood lines because LR contains calcium.0.9% Saline Preferred isotonic crystalloid solution for head trauma. Only solution used in blood transfusionlines and to dilute pRBCs. May cause hyperchloremic metabolic acidosis (with normal anion gap) due toexcess chloride displacing serum HCO3.

HespanHigh-molecular-weight hetastarch. Hextend (6% hetastarch High-molecular-weighthetastarch. HalfNot recommended because of adverse effects on(6% hetastarch in 0.9% saline) Half-life, 30 hours. Abandoned at authors institution-life, 30 hours. Less coagulopathy and platelet dysfunctionin balanced electrolyte solution) compared with Hespan. Maximum dose, 1015 mL/kgLow- and medium-molecular- Colloid solutions with less coagulopathy and platelet dysfunction comparedwith high-molecularweight

hetastarch weight hetastarch. Low-molecular-weight hetastarch associated with improved muscle oxygentension, lower markers of inflammation, and endothelial activation compared with LR. Availablein Europe and Canada. Not currently available in United States.Albumin (5%) Little effect on coagulation. May pass into interstitial compartment if impaired vascularintegritywith resultant endothelial swelling and impaired microcirculatory perfusion. Increased mortalityafter head trauma in SAFE study (vs. 0.9% saline).46Dextrans and gelatins Colloid solutions largely abandoned in United States because of negative effects on

coagulationand potential for anaphylaxis and hypersensitivity reactionsHypertonic saline Variety of solutions/concentrations. May be combined with colloid to prolong duration ofaction.Efficiently restores intravascular volume and decreases extravascular volume and tissue edema.Decreases ICP and increases CPP. Especially advantageous in prehospital situations and in headtrauma with refractory increased ICP. Not associated with improved neurologic outcomes


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There is controversy concerning which intravenous solutionsshould be used for resuscitation .

During hemorrhage, a compensatory increase inreabsorption of fluid into capillaries partially restores theintravascular compartment, but depletes the interstitialspace.

To replete the intravascular and interstitial compartments,crystalloid solutions such as isotonic 0.9% saline or lactatedRingers (LR) solution are traditionally used.

Glucose-containing solutions are avoided becausehyperglycemia is associated with aggravation of centralnervous system injuryand increased mortality, especially intrauma patients.


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The effects of crystalloid solutions on the coagulation

system are complex.

With hemodilution up to 20 to40%crystalloids produce ahypercoagulable state because of dilution of

anticoagulant factors such as antithrombin and byplatelet activation.

After 60% hemodilution, both crystalloids and colloidsproduce a hypocoagulable state.


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One unit of packed RBCs will usually increase thehematocrit by approximately 3% or the hemoglobin by 1

g/dL in a 70-kg nonbleeding adult

If 50% to 75% of the patient's blood volume has been

replaced with type 0 blood (e.g., approximately 10 unitsof red cells in an average size adult patient), one shouldcontinue to administer type O red cells. Otherwise, riskof a major cross-match reaction increases because thepatient may have received enough anti-A or anti-B

antibodies to precipitate hemolysis if A, B, or AB unitsare subsequently given.


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Approach to Transfusing Red Blood Cells (RBCs)Based on the American Society of AnesthesiologistPractice Guidelines and Review of the Literature. Transfuse RBCs if hemoglobin 10 g/dL Decision to transfuse RBCs should be individualizedbased on:

1. Presence of organ ischemia (e.g., altered mental status,myocardial ischemia, acidosis, low mixed venous oxygensaturation)2. Rate of bleeding

3. Magnitude of bleeding4. Intravascular volume status5. Cardiopulmonary reserve

Coagulation Factors and Platelets


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Coagulation Factors and Platelets

Two units of fresh-frozen plasma (1015 mL/kg) will achieve30% factor activity in most adults

The primary cause of bleeding after trauma is surgical, while thesecond leading cause is hypothermia and dilutional coagulopathy

Cryoprecipitate and factor concentrates may be indicated tocorrect specific factor deficiencies. Cryoprecipitate is rich infibrinogen as well as factors VIII, XIII, and von Willebrand factor.

Thrombocytopenia is treated with platelet concentrates

Platelet transfusions are usually indicated in the presence of clinicalbleeding and a platelet count


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COAGULATION MONITERING

PT

APTT

FIBRINOGEN

FDP

THROMBOELASTOGRAM


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Definitions of MassiveTransfusion

One blood volume loss in 24 hours (equivalent to 10

units of whole blood )

Four or more units replaced in 1 hour with continuingbleeding

50% blood volume loss in 3 hours (equivalent to 5 unitsof whole blood)

50 units lost in 48 hours

20 units lost in 24 hours

Blood loss exceeding 150 mL/min.


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The adverse effects of hypothermia in the trauma patientinclude

major coagulation derangements, peripheral vasoconstriction, metabolic

acidosis, compensatory increased oxygen requirements during rewarming,and impaired immune response.

Standard coagulation tests are temperature-corrected to 37C and maynot reflect hypothermia-induced coagulopathy. Hypothermia impairscoagulation because of slowing of enzymatic rates and reduced platelet

function.Even worse, different steps in coagulation cascade are affected to

different degrees, disrupting synchronization of the cascade.Hypothermia can cause cardiac dysrhythmias and even cardiac arrest

from electromechanical dissociation, standstill, or fibrillation, especially with

core temperatures below 30C.Hypothermia also impairs citrate, lactate, and drug metabolism;

increases blood viscosity; impairs RBC deformability; increases intracellularpotassium release; and causes a leftward shift of the oxyhemoglobindissociation curve. A mortality of 100% has been reported in trauma patientswhose body temperature fell below 32C,


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Resuscitation End Points

Within the First 24 Hours afterTrauma

Parameter Value

Mixed venous oxygen tension >35 mm Hg

Mixed venous oxygen saturation >65%

Base deficit > -3 mmol/L

Lactate


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Goals for Fluid Resuscitation

Achievement of normovolemia and hemodynamic stability

Correction of major acid-base disturbances

Compensation of fluxes from the interstitial/intracellularcompartments

Improvements of microvascular blood flow

Prevention of activation of inflammatory cascade system

Normalization of oxygen delivery to tissue cells and cell

metabolism

Prevention of reperfusion injury


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capacitance, and positive inotropic effects through direct actions onmyocardial cells

Hypertonic solutions and hypertonic/hyperoncotic solutions may improvecardiovascular function on multiple levels: displacement of tissue fluid into

the blood compartment, direct vasodilatory effects in the systemic andpulmonary circulation, reduction in venous

Because of the hypertonicity of the solutions,only a small volume offluid (approximately 4 mL/kg) is necessary to effectively restore

cardiovascular function (small-volume resuscitation).


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Improved microperfusion resulting frominfusion of hypertonic solutions (small-volume resuscitation).


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In inflammatory-related capillary leak, HEShas been reported tohave occlusiveeffects on damagedcapillaries,subsequently limitingthe extravasation of fluid. LMW HES may

exert benefical effects on endothelialfunction by stabilization of fragile cellmembranes or by avoiding endothelial

swelling This may be of benefit in thosetrauma patients suffering from severeendothelial leakage


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Management of bleeding patients with fluids andblood/blood products


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Risks Associated with Allogeneic TransfusionOnset Time Mechanism Complication

Acute Immunologic Acute hemolyticAllergic/anaphylactoidTransfusion-related acute lunginjury (TRALI)FebrileInfectious Bacterial contamination

Metabolic Volume overloadStorage defect-associated injuryDelayed Immunologic Delayed hemolyticPosttransfusion purpuraGraft-versus-host diseaseTransfusion-related

immunomodulation (TRIM)Infectious Viruses, parasites, prionsOncogeneMetabolic Iron overload


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these echinocytes do not pass through capillaries in thesame fashion as do normal,unstored cells

During the storageof a red cell, red cell shape change occurs due to areduction in intracellular adenosine triphosphate, sialic

acid, and nitric oxide.

After approximately 14 days of storage, dependent on thestorage solution, the red cells lose their biconcave disc

shape and become echinocytes


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Diagnosis of Transfusion-Related Acute Lung Injury1. No acute lung injury prior to transfusion

2. Acute lung injury occurs during or within 6 hours oftransfusion

3. Acute onset of respiratory distress

4. Hypoxemia

5. Bilateral lung infiltrates on chest radiograph

6. No evidence of circulatory overload

7. No other acute lung injury risk factors (septic shock,sepsis, aspiration, lung contusion, pneumonia, multiple trauma,drug overdose, burn injury, cardiopulmonary bypass, inhalationinjury, acute pancreatitis) overload


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A DEDICATED TRAUMA TEAM CAN SAVE THIS LIMB


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Resusitation in Trauma