TRAUMA TOPICS
From Los Angeles County/University of Southern California Medical Center’s Trauma and Critical Care Symposium
Educational Objectives
| The goal of this program is to improve outcomes and reduce mortality among trauma patients. After hearing and assimilating
this program, the clinician will be better able to:
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 | 1. Discuss strategies for hemostasis and compare available hemostatic dressings.
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| 2. Identify patients with head injuries likely to require repeat computed tomography.
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| 3. Analyze treatment outcomes to identify preventable complications and reduce errors.
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| 4. Describe the risks and benefits associated with steroid therapy for patients with spinal cord injuries.
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| 5. Discuss the role of factor VIIa in the treatment of trauma patients.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the planning committee
to disclose relevant financial relationships within the past 12 months that might create any personal conflicts of interest. Any identified
conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business or
commercial interest. For this program, the faculty and planning committee reported nothing to disclose.
Acknowledgments
Drs. Jurkovich, Cornwell, Inaba, Putnam, and Sise were recorded at 15th Annual USC Trauma/Critical Care Symposium,
sponsored by the Keck School of Medicine at the University of Southern California, and Department of Nursing, Los
Angeles County/USC Medical Center, and held May 12-13, 2008, in Pasadena, CA. The Audio-Digest Foundation
thanks the speakers and the sponsors for their cooperation in the production of this program.
| HEMOSTASIS: NEW THERAPIES —Gregory J. Jurkovich, MD, Professor of Surgery, University of Washington
School of Medicine, and Chief of Trauma Services, Harborview Medical Center, Seattle
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| Hemorrhage control: uncontrolled bleeding—important preventable cause of death among trauma patients; responsible
for 40% of trauma deaths, 60% of which occur in hospital; direct control of bleeding—silk ligatures, clamps, and
tourniquets; angiographic embolization; packing; enhancement of endogenous clotting mechanisms—use of native
blood products (eg, cryoprecipitate, platelets) and specific factors (eg, recombinant factor VIIa); more strategies for extrinsic
control—direct pressure; surgery and ligation; resuscitation strategies; topical agents —adjunctive approach to
hemorrhage control (do not replace standard techniques)
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| Thrombin and fibrinogen: form basis for clotting by providing matrix to which platelets attach; agents often combine
bovine thrombin with human fibrinogen (pooled source); sealant dressing covers raw surfaces and stimulates
endogenous clotting mechanisms
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| Products: Tisseel—fibrinogen and thrombin pooled from human donors (raises questions about safety); preparation includes
stirring and warming for ≈20 min (ie, not appropriate in emergency settings); approved for cardio-pulmonary
bypass, splenic injury, and colostomy cultures; mixture sprayed over wound; Floseal—gelatin matrix (using bovine
collagen) with human thrombin; no mixing or warming required; sprayed on wound; improves clotting and reduces
bleeding from oozing anastomoses; also used in cardiac surgery (eg, bypass grafting, valve replacement); Evicel—
human thrombin and fibrinogen; product does not contain aprotinin (additive that may cause intense allergic reactions;
note, to prevent anaphylactic reaction, avoid using products with aprotinin for 12 mo after initial exposure);
most effective when used for microvascular clotting (eg, vascular anastomoses); some thrombotic effect when used
in open wounds; recombinant thrombin—contains no human thrombin; as effective as bovine thrombin (which stimulates
formation of antibodies and may cause allergic reaction or delayed serum sickness); recombinant form more
expensive, but does not stimulate allergic response
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| Risk: thrombosis may occur if thrombin absorbed systemically; thrombin-containing products must not be injected directly
into blood vessel (may lead to thrombotic necrosis); contraindication—known hypersensitivity to thrombin
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| Use: inappropriate to use for massive arterial bleeding; best used for oozing blood vessels and minor bleeding from
capillaries
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| Hemostatic bandages: original products made of fibrin sheets and powders and packed into wounds; dry fibrin sealant
dressing (DFSD)—contains fibrinogen, thrombin, factor XIII, and calcium; not currently approved by Food and
Drug Administration (FDA); Rapid Deployment Hemostat (RDH)—uses proprietary polysaccharide derived from
marine microalgae; increases local concentration of platelets and clotting factors and induces vasospasm; FDA-approved;
chitosan dressing—deacetylated polysaccharide adheres strongly to wounds and concentrates platelets;
FDA-approved; QuikClot—widely used in prehospital setting; made with granular zeolite (synthetic derivative of
volcanic rock); produces heat when exposed to water; FDA-approved
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| Efficacy (animal studies): DFSD—reduces loss of blood and improves survival (but no better than gauze packing);
RDH—improves mean arterial pressure, levels of lactate and hemoglobin, and hematocrit; chitosan dressing—
reduces blood loss and need for transfusion or fluids and improves survival (compared to gauze control)
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| WHO NEEDS REPEAT HEAD COMPUTED TOMOGRAPHY (CT) AFTER TRAUMATIC BRAIN INJURY ?—
Edward E. Cornwell III, MD, LaSalle D. Leffall Jr. Professor and Chair, Department of Surgery, Howard University College
of Medicine, Washington, DC
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| Guidelines: evidence-based guidelines pertain to patients with Glasgow Coma Scale (GCS) scores ≤8; no guidelines for
patients with less severe injuries; important to identify patients at risk for secondary brain trauma, recurrent bleeding, or
increased intracranial pressure (ICP)
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| Hypotension and hypoxemia: mediators of secondary brain injury after trauma; associated with decreased survival
(25%-37% vs ≈75% among patients without hypotension or hypoxemia)
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| Risk for intracranial hypotension: patients with GCS ≥13 have low (1%-2%) risk; patients with GCS of 9 to 12 have intermediate
(≥10%) risk (generally do not require monitoring of ICP); patients with GCS ≤8 plus abnormal findings on
CT have high (\>50%) risk (ICP monitoring device recommended); patients with normal findings on CT—those with
GCS ≤8 and 2 of 3 risk factors (age \>40 yr; posturing [eg, asymmetric examination; blown pupil; unilateral or bilateral
posturing]; hypotension on admission) require monitoring of ICP and repeat head CT; patients at risk for recurrent
bleeding and intracranial hypertension, even if they appear clinically stable
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| Advanced age: cerebral atrophy common; blood may accumulate in intracranial vault without causing acute increase
in ICP, shifting of midline, or other signs of intracranial hypertension, potentially delaying diagnosis of brain hemorrhage;
older patients also commonly take antiplatelet agents, which inhibit clotting; speaker’s recommendations—
repeat head CT recommended for patients with abnormal examination or abnormal findings on initial CT, even if head
injury appears minor; if no abnormal findings on examination or CT, observe patient without performing repeat CT
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| PREVENTABLE COMPLICATIONS AND DEATHS: LESSONS LEARNED AT A MATURE TRAUMA CENTER —
Kenji Inaba, MD, Assistant Professor of Surgery, Medical Director, Surgical Intensive Care Unit, and Program Director,
Surgical Critical Care Fellowship, the Keck School of Medicine of the University of Southern California, Los Angeles
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| History: tracking outcomes and assessing reasons for treatment failure first promoted by Dr. Ernest Codman (founding
member of American College of Surgeons [ACS] and Committee for Hospital Standardization [predecessor to Joint
Commission for the Accreditation of Healthcare Organizations]); Codman Hospital established public reporting of
complications and deaths
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| Preventable complications: key benchmark of quality improvement in trauma setting; identifying preventable complications
and tracking changes in error rates allows assessment of protocols and systems; important part of ACS verification
for trauma centers
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| Trauma center experience: \>35,000 trauma patients treated at speaker’s institution from 1998 to 2005; 2560 complications
identified and reviewed; 8% of complications considered “potentially preventable,” and 7% considered “preventable”
(groups pooled for data analysis); 351 patients experienced 403 preventable complications; ratio of
nonpreventable to preventable complications remained relatively consistent over time; types of complications—airway
(≈25%; unintended extubation most common); complications detected postoperatively (≈25%; primarily technical failures,
eg, failed anastomoses); delayed diagnosis (≈20%; eg, missed injuries); complications associated with catheters,
drains, or tubes (≈20%); complications detected intraoperatively (≈10%; eg, iatrogenic injury to organs); others (eg,
mismanagement of medication or fluids); clinical impact—64% of preventable complications led to changes in management
to reduce error rates; “July phenomenon”—at teaching institutions, health care team includes many trainees
with diverse levels of experience; retrospective analysis of data collected over 5 yr showed nonsignificantly higher
rates of mortality and doubled rates of preventable complications and errors (0.6% vs 1.1%) at beginning of academic
year, compared to end of academic year
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| STEROIDS FOR SPINAL CORD INJURY —Brant A. Putnam, MD, Assistant Professor of Surgery, the David Geffen
School of Medicine at the University of California, Los Angeles, and Chief, Trauma/Surgical Critical Care, Harbor-
UCLA Medical Center, Los Angeles
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| Pathophysiology of spinal cord injury (SCI): primary cell death—occurs at time of injury; caused by mechanical
forces (eg, shear, breakage, compression), resulting in disruption of neurons, support cells, and vascular structures; initiates
inflammatory cascade; secondary cell death—progresses over days to weeks; involves local hypoxia and ischemia,
changes in ion (eg, Ca2+ ) influx, lipid peroxidation, and production of free radicals; generation of inflammatory
mediators responsible for secondary cell death; methylprednisolone—high doses may prevent lipid peroxidation and
generation of free radicals; some data suggest role in preventing apoptosis of oligodendrocytes and other support cells in
injured area
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| Clinical trials: North American Spinal Cord Injury Study (NASCIS) I—multicenter randomized double-blind trial compared
effects of low- and high-dose methylprednisolone among 330 patients with spinal cord injuries; ≈50% of patients
followed for 6 mo; no difference in neurologic improvement (motor or sensory) between groups; high-dose
group had significantly higher rate of wound infections, and nonsignificantly higher rates of sepsis, pneumonia, and
pulmonary embolus; NASCIS II—placebo-controlled study of almost 500 patients showed no overall differences in
neurologic outcomes; post hoc analysis showed that patients who received steroids ≤8 hr after injury had some motor
improvements at 1 yr (compared to those receiving delayed delivery of steroids); patients receiving steroids had nonsignificantly
increased rates of wound infection and pulmonary embolus; findings led to adoption of high-dose steroids
as treatment of choice for patients with SCI; American Spinal Injury Association (ASIA) score—motor score
based on 10 groups of motor function; sensory score based on pin prick and light touch; in NASCIS II, steroid treatment
associated with 5-point improvement on motor score (may reflect 5-point improvement in 1 muscle group or 1-
point improvement in 5 muscle groups); NASCIS III—compared 2 durations of steroid therapy (24 hr and 48 hr); all
patients received bolus of methylprednisolone and treated within 8 hr of injury; no differences in outcomes seen between
groups; post hoc analysis showed modest benefit (5- to 6-point improvement in motor score) associated with
48-hr protocol at 6 wk and 6 mo, but effect disappeared by 1 yr; longer treatment duration associated with higher incidence
of complications
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| Criticisms: results released to media before published in peer-reviewed journals; modest improvements have questionable
clinical significance; public pressure and absence of other options led to adoption of steroids as standard of care,
but neither NASCIS II nor III found differences in primary outcomes; authors refused independent review of data;
statistical analysis questioned; treatment associated with increase in septic complications
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| Disadvantages of steroids: wound infection; pneumonia; gastrointestinal bleeding; hyperglycemia
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| Practice patterns: many physicians who use steroids in setting of SCI do not follow specific protocol; survey showed
physicians vary widely in opinion about appropriateness of steroid therapy for patients with SCI, and that those who
used steroids do so because of belief of benefit; other concerns—steroids linked to development of myopathy
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| Position statements: use of steroids for acute SCI labelled as treatment option, but not standard of care or guideline;
most recent independent evidence-based review cites insufficient evidence to support use of methylprednisolone as
standard treatment for patients with acute SCI
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| Take-home message: prevent secondary injury by adequately immobilizing patient and avoiding hypoxia and hypotension
(adequate blood perfusion important); prompt surgical intervention required for mass lesions; consider methylprednisolone
as option, but recognize risks
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| FACTOR VIIA: EARLY, LATE, OR NOT AT ALL ?—Michael J. Sise, MD, Clinical Professor of Surgery, University
of California, San Diego, School of Medicine, and Trauma Medical Director, Scripps Mercy Hospital, San Diego
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| Factor VIIa: mechanism of action—has central role in clotting cascade; binds tissue factor at injury site; initiates coagulation
with thrombin burst, limited to site of injury; use—approved for use only in patients with hemophilia; widely used
under “compassionate use” guidelines in trauma settings
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| Evidence: swine model—treatment with factor VIIa resulted in improved blood pressure, prothrombin time (PT), and
survival; clinical experience—case series of 81 patients showed efficacy in correcting PT, but survival did not improve;
posssible selection bias because treatment given only to seriously injured patients; treatment ineffective among patients
with prolonged PT or very severe injuries; randomized controlled trials—treatment associated with reduced rate of
transfusions and promising trend in mortality (but no proven benefit); military experience—treatment associated with
fewer transfusion units; no effect on risk for acute respiratory distress syndrome (ARDS), infection, thrombosis, or
mortality; other studies—benefit suggested among patients with coagulopathy or head injury
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| Precautions and contraindications: ineffective in hypothermic or acidotic patients; safety—relatively high risk for
thrombotic complications (eg, stroke; mesenteric or peripheral thrombosis); lower-dose regimen safer; other issues—
high cost
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| Current practice: used broadly with little control; benefit mostly based on anecdotal results, but few alternatives exist;
factor VIIa used less frequently, due in part to current practice of using 1:1 ratio of packed cells to fresh frozen
plasma (FFP); standard approach and outcome measures needed; experience with 1:1 resuscitation—since adopting
practice, speaker’s institution has used factor VIIa only once in trauma patient
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| Recommendations: protocols for massive transfusions have changed over time; earlier protocols found to cause harm;
prudent evidence-based practice important, but evidence limited; absolute indication—medical coagulopathy; general
guidelines—resuscitate with 1:1 or 1:2 ratio of packed cells to FFP; follow laboratory and clinical status; carefully consider
use of factor VIIa; use low-dose regimen and keep good record of use; consider appointing individual to make decision
about using factor VIIa; carefully review resuscitation to ensure appropriate use; take-home message—early use
appropriate for patients with medical coagulopathy and possibly for those in hemorrhagic shock; late use appropriate
for patients with refractory coagulopathy; in general, decrease use of factor VIIa
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Suggested Reading
Boffard KD et al: Recombinant factor VIIa as adjunctive therapy for bleeding control in severely injured trauma patients: two
parallel randomized, placebo-controlled, double-blind clinical trials. J Trauma 59:8, 2005; Brown CV et al: Indications for
routine repeat head computed tomography stratified by severity of traumatic brain injury. J Trauma 62:1339, 2007; Cohen DB
et al: Traumatic brain injury in anticoagulated patients. J Trauma 60:553, 2006; Compagnone NA: Treatments for spinal
cord injury: is there hope in neurosteroids? J Steroid Biochem Mol Biol 109:307, 2008; Dutton RP et al: Factor VIIa for correction
of traumatic coagulopathy. J Trauma 57:709, 2004; Forster AJ et al: Adverse events following an emergency department
visit. Qual Saf Health Care 16:17, 2007; Kozen BG et al: An alternative hemostatic dressing: comparison of CELOX,
HemCon, and QuikClot. Acad Emerg Med 15:74, 2008; Lynn M et al: Early use of recombinant factor VIIa improves mean
arterial pressure and may potentially decrease mortality in experimental hemorrhagic shock: a pilot study. J Trauma 52:703, 2002;
Mayer SA et al: Efficacy and safety of recombinant activated factor VII for acute intracerebral hemorrhage. N Engl J Med
358:2127, 2008; Miller SM: methylprednisolone protects oligodendrocytes but not neurons after spinal cord injury. J Neurosci
28:140, 2008; Pronovost PJ et al: The wisdom and justice of not paying for “preventable complications”. JAMA 299:2197,
2008; Smith JS et al: The role of early follow-up computed tomography imaging in the management of traumatic brain injury
patients with intracranial hemorrhage. J Trauma 63:75, 2007; Stein DM et al: Low-dose recombinant factor VIIa for trauma
patients with coagulopathy. Injury 39:1054, 2008; Stewart RM, Corneille MG: Common complications following thoracic
trauma: their prevention and treatment. Semin Thorac Cardiovasc Surg 20:69, 2008; Zeller J et al: Beyond the battlefield.
The use of hemostatic dressing in civilian EMS. JEMS 33:102, 2008.
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