TRAUMA UPDATE
Selections from Critical Care, presented July 2005 by the University of California, San Diego, School of Medicine
| BURN RESUSCITATION —Bruce Potenza, MD, Associate Professor of Surgery, University of California, San Diego,
School of Medicine
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| Initial evaluation: type of burn, eg, explosion, flame, contact; duration of exposure to burn-causing agent; whether burn
sustained in closed space, ie, likelihood of inhalation injury (uncommon if burn sustained outside); steps taken by paramedics
to alleviate burn
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| Burn severity: superficial partial thickness (superficial second degree)—burn extends from epidermal layer into superficial
dermis; deep partial thickness—burn extends into dermis; full thickness—burn extends all the way down; fourth
degree—burn extends into fat, muscle, or bone; implications—if hair follicles and sweat appendages intact, epithelial
buds germinate new skin; typically, superficial second-degree burn with blistering heals well; deep partial-thickness
burns partially compromise germinal areas, so burn may or may not heal
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| Burn shock: systemic manifestation of burn; inadequate end-organ and cellular perfusion; blood diverted from organs that
can better withstand ischemia to maintain perfusion to heart, lung, brain, and kidneys
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| Pathophysiology: rapid edema formation can result in airway compromise, prerenal azotemia, or in patients with bigger
burns, depressed myocardial contractility; capillary permeability—as burn mediators pass through capillary junctions,
junctions increase in size; macromolecules within capillaries can pass through enlarged junctions; albumin leaking into
interstitium increases oncotic pressure and draws more fluid into edematous area; edema progression—maximal edema
formation occurs in 8 hr with small burns and 24 hr with large burns
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| Effects of delayed resuscitation: prerenal syndrome with intravascular volume contraction due to edema; initial increase
in cardiac output until maximal level of tachycardia reached; initial increase in systemic vascular resistance, which can
become vasodilatation or systemic inflammatory response syndrome with continued delay; decreased perfusion affects
kidneys; exacerbation of ongoing metabolic acidosis
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| Burn shock mediators: histamines—increase capillary permeability; prostaglandins—cause vasoconstriction and contribute
to vasodilatation; bradykinins—cause profound separation of cell junctions at capillary endothelium, leading to
capillary leak; thromboxane and catecholamines—cause vasoconstriction at capillary bed level, leading to poor perfusion
and increase in ongoing ischemia; superoxide radicals—assist in degradation of cell walls
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| Fluid resuscitation: Parkland formula—4 mL/kg x % burn, eg, 70-kg man with 20% burn requires 4 x 70 x 20 mL of
fluid in 24 hr (half in first 8 hr); crystalloid resuscitation—Lactated Ringer’s solution provides 130 mEq of sodium
(similar to interstitial edema component); hypertonic resuscitation—speaker adds 50 mEq of sodium chloride to give
slightly hypertonic solution with 180 mEq of serum sodium; trend toward using more hypertonic fluids and resuscitation
with 3% saline; albumin—not administered in first 24 hr because known to leak into interstitium; child resuscitation
formula—3 to 4 mL/kg; inhalation component—more fluid added; small burns—maintenance fluids sufficient;
children—maintenance (including glucose solution) and resuscitation fluids required
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| Monitoring resuscitation: monitor blood pressure (BP), pulse, urine output, mental status, acid-base status, and hematocrit
(aim to get level slightly below baseline); do not use bolus of fluid because it will increase hydrostatic pressure and
force it into interstitium; increase and decrease rate of fluid administration in steps of 200 mL; high urine output (0.5 mL/
kg in adults, 1-2 mL/kg in children) can be misleading because factors such as atrial natriuretic peptide can cause artificially
high output; raise head of bed to decrease severe facial edema; secure adequate airway; secure intravenous (IV) access
early
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| Compartment syndrome: extremities—usually due to circumferential burns; evidenced by decreased capillary refill and
decreased pulse; patient may or may not complain of paresthesias and pain; abdomen—after resuscitation, fluid-filled
abdomen can cause problems, eg, diaphragm unable to descend; tidal volumes, urine output, and cardiac output decrease;
airway pressure increases
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| Smoke inhalation: combination of thermal injury and chemical injury due to toxic byproducts or particulate matter; few
patients get severe thermal injuries because of cooling mechanism provided by nose and hypopharynx; most problems
due to soot, dust, or chemical pneumonitis from toxic breakdown; evaluation—assess baseline arterial blood gas and
carboxyhemoglobin (Hbco) levels; Hbco >10% indicates fire damage; treatment—administer 100% fraction of inspired
O2 for 4 to 6 hr; treatment in hyperbaric chamber indicated if Hbco >25%
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| ROLE OF ORTHOPEDIC SURGERY IN THE MANAGEMENT OF TRAUMATIC SHOCK —Alexandra Schwartz,
MD, Assistant Professor of Surgery, Chief of Orthopedic Trauma, University of California, San Diego, School of Medicine
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| Traumatic shock: hypovolemia due to hemorrhage; systolic BP <90 mm Hg traditional definition; young patients can
present with compensated shock, ie, without hypotension but with tachycardia, mental status changes, and diaphoresis;
elderly patients on β-blockers do not present with typical tachycardic response
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| Sources of bleeding: abdomen; chest; retroperitoneum; blood left behind on street; multiple fractures; pelvic fractures
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Open Fractures
| Assessment: inspect immediately after assessment of airway, breathing, and circulation (ABC); remove splint if already applied
to facilitate inspection of injury; open fractures continue to ooze until bone stabilized; direct pressure preferred to suture
ligation or clamping because blood vessels situated near nerves
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Multiple Fractures
| Potential blood loss: humerus and tibia 750 mL; femur 1.5 L; pelvis 2 L
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| Stabilization: stabilize with splint or traction to help realign bone and reduce compartment volume and blood loss
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Pelvic Fractures
| Mortality: 40%; uncontrolled pelvic bleeding related to 40% of deaths; factors increasing mortality—disruption of posterior
ring (sacrum, sacroiliac [SI] joints); high injury severity score; hemorrhagic shock on admission; large blood requirement;
perineal lacerations or open fractures; age (mortality increases with age)
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| Open pelvic fractures: mortality rate 50%; often present with perineal wound; perform early diverting colostomy if colon,
rectum, or perineal injury present; irrigate and close vaginal laceration early to prevent abscess formation; debride soft-
tissue wounds aggressively but wait to close
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| Urologic injuries: incidence 15%; classically present as blood at meatus or high-riding prostate, leading to swelling of
scrotum or labia; retrograde urethrography indicated if urologic injury suspected (wait to perform if patient hemodynamically
unstable, because dye extravasation can interfere with angiography and radiography)
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| Radiography: anteroposterior (AP) pelvis—line where sacrum and ilium meet should be smooth; 2 superior rami should
be apposed and level; line from femoral neck around obturator foramen should be congruent (noncongruent line indicates
hip dislocation); inlet view—tilt x-ray beam 45° from cephalad to caudad; displays widest dimension of pelvis (end-on
view); shows anterior-posterior translation and SI joints; outlet view—displays vertical component of pelvis; shows superior-inferior
translation
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| Computed tomography (CT): use 5-mm cuts through pelvis (3-mm cuts if acetabular fracture involved); aids visualization
of posterior pelvis, sacral fractures, SI joint injury, and nerve root involvement
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| Stable fractures: low-energy injuries, eg, falling; injury with one fracture line considered stable; examples—iliac wing
fracture; nondisplaced fractures
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| Unstable fractures: high-energy injuries; almost always displaced and involve >1 fracture; anything involving front and
back of pelvis; if pelvis rocks when squeezed, patient has mechanical instability; patients with mechanical instability can
have hemodynamic instability; radiographic signs—SI joint widened by 5 mm; gap in back of pelvis; avulsion fracture of
L5 vertebra (pelvic ligaments attach at L5); symphysis 2.5 cm wide
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 | AP compression (“open book”): usually involves force from front causing external rotation of leg; if anterior ligaments
tear but posterior ligaments intact, patient unlikely to have unstable pelvis; if posterior ligaments tear, pelvis becomes
unstable; usually involves wide symphysis in front and wide SI joints in back; aortic tears—associated with AP pelvic
fractures; studies show patients with pelvic fractures have 2- to 5-fold increase in aortic rupture; study—in >4000
patients with blunt trauma, 12 aortic ruptures reported; 10 (>80%) of 12 ruptures occurred in patients with AP compression
injury
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| Lateral compression: force from side folds pelvis in on itself, leading to sacral fracture and fracture in front; sufficient
force can cause “windswept pelvis,” where half of pelvis rotates internally and causes other half to rotate externally
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| Vertical shear: almost always associated with severe vascular injury; pelvis displaced proximally and posteriorly, tearing
all ligaments; always unstable
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| Hemorrhage control: average blood replacement for lateral compression 6.5 units (all other injuries require much more);
mortality 38% for hemodynamically unstable patients, compared to 3% for stable patients
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| Cause of death: head injury major cause of death in patients with lateral compression pelvic fracture; visceral injury or internal
bleeding from pelvis major cause of death in patients with AP fracture
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| Stabilization options: bed sheet; binders; sand bags; angiography; external fixation; pelvic packing; definitive fixation;
pelvic sheet—closes volume and prevents oozing from bony surfaces; keep sheet flat and secure with clamps; avoid
knots, because they can erode skin; angiography—absolute indications include failed resuscitation or no pulse; effects
of stabilization—controls bleeding; helps with patient positioning and mobilization; decreases pain
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| WHAT’S NEW IN SEPSIS —Raul Coimbra, MD, PhD, Associate Professor of Surgery and Director of Surgical Intensive
Care Unit, University of California, San Diego, School of Medicine
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| Consensus Conference definitions (1991): systemic inflammatory response syndrome (SIRS)—complex findings that
result from systemic activation of immune response; clinical parameters—body temperature >38°C or <36°C; tachycardia;
respiratory rate >20/min; low PCO 2 ; leukocytosis or leukopenia; sepsis—SIRS plus infection; severe sepsis—
sepsis associated with organ dysfunction, hypoperfusion, or hypotension; septic shock—sepsis with arterial hypotension
unresponsive to fluid resuscitation
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| Early goal-directed therapy (Rivers et al): 263 patients with SIRS, hypotension, and elevated lactate randomized to
standard therapy or goal-directed therapy instituted in emergency department and continued for 6 hr before transfer to intensive
care unit (ICU); standard resuscitation—patients received arterial and central venous (CV) lines; goal to maintain
mean arterial pressure (MAP) >65 mm Hg, adequate urine output, and adequate central venous pressure (CVP);
early goal-directed therapy—patients received arterial catheter and CV catheter capable of measuring CV O2 saturation;
protocol—patients resuscitated with fluids to maintain CVP at 8 to 12 mm Hg; if MAP <65 or >90 mm Hg, vasoactive
agents administered; if CV O2 saturation <70%, red blood cells transfused to hematocrit of 30%; transfusion
stopped when CV O2 saturation >70%; inotropic medications considered if CV O2 saturation remained <70%; if goals
achieved, patient admitted to ICU; if goals not achieved, protocol repeated; results—early goal-directed therapy resulted
in significant decrease in hospital mortality (30.5%), compared to standard therapy (46.5%)
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| Activated protein C: 2 prospective randomized trials demonstrated efficacy of drotrecogin alfa (activated protein C; Xigris)
for reduction of mortality in patients with sepsis; mechanism of action—decreases inflammation, coagulation, and
microvascular thrombosis, resulting in improved circulatory blood flow to tissues and subsequent reduction in multiple
organ failure; indications—patients at high risk for death (Acute Physiology and Chronic Health Evaluation [APACHE]
II score >25 or requiring vasopressors); clinical trials summary—drotrecogin alfa associated with mortality rate of 31%
(44% for standard therapy), relative risk reduction of 29%, improved MAP, improved oxygenation, and decreased time
on mechanical ventilation; timing—if drotrecogin alfa administered on day 1 after diagnosis, mortality reduction realized;
if administered on day 2 or 3, effect reduced; side effects—increased risk for bleeding, particularly in postoperative
and trauma patients and those with head injuries
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| Protective lung strategies: Amato et al—protective lung strategies effective at decreasing mortality in patients with
acute respiratory distress syndrome (ARDS) secondary to sepsis; patients ventilated with lower tidal volume, accepting
risk for some degree of permissive hypercapnia; patients displayed less barotrauma and pneumothorax; Acute Respiratory
Distress Syndrome Network (ARDSNet) trial—reduction of tidal volume from 12 to 6 mL/kg and plateau pressure
from 50 to 30 cm H2 O associated with significant decrease in mortality
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| Intensive insulin therapy: study—mortality rate reduced from 8% to 4.6% if glucose maintained at 80 to 110 mg/dL;
death due to multiple organ failure with septic focus decreased most
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| Low-dose corticosteroids: study—patients randomized to IV hydrocortisone 50 mg q6h and fludrocortisone 50 µg qd or
matching placebo for 7 days; mortality reduced from 63% to 53% in corticosteroid group; no decrease in adverse events;
immune suppression not associated with low-dose corticosteroids
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| Other methods of preventing sepsis in ICU: limit blood transfusion; limit antibiotic use; aggressive enteral nutrition;
limit parenteral nutrition
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Educational Objectives
| The goal of this program is to educate the listener on issues in trauma surgery. After hearing and assimilating this program,
the clinician will be better able to:
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| 1. Review burn shock.
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| 2. Explain resuscitation in burn patients.
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| 3. Describe the role of orthopedic surgery in the management of traumatic shock.
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| 4. Evaluate and treat pelvic fractures.
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| 5. Discuss treatment options for sepsis.
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Discussed on This Program
Albumin human (normal serum albumin), 5% [several trade names]
Drotrecogin alfa (activated protein C) [Xigris]
Fludrocortisone acetate [Florinef Acetate]
Hydrocortisone (cortisol) [several trade names]
Lactated Ringer’s solution (Dextrose electrolyte solution)
Suggested Reading
Acute Respiratory Distress Syndrome Network: Ventilation with lower tidal volumes as compared with traditional tidal
volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 342:1301, 2000; Annane D et al:
Effect of low doses of corticosteroids in septic shock patients with or without early acute respiratory distress syndrome. Crit
Care Med 34:22, 2006; Balogh Z et al: Institutional practice guidelines on management of pelvic fracture-related hemodynamic
instability: do they make a difference? J Trauma 58:778, 2005; Barrow RE et al: Early fluid resuscitation improves
outcomes in severely burned children. Resuscitation 45:91, 2000; Bellabarba C et al: Midline sagittal sacral fractures in
anterior-posterior compression pelvic ring injuries. J Orthop Trauma 17:32, 2003; Bernard GR et al: Extended evaluation
of recombinant human activated protein C United States Trial (ENHANCE US): a single-arm, phase 3B, multicenter study of
drotrecogin alfa (activated) in severe sepsis. Chest 125:2206, 2004; Britt RC et al: Secondary abdominal compartment syndrome:
risk factors and outcomes. Am Surg 71:982, 2005; Cartotto RC et al: How well does the Parkland formula estimate
actual fluid resuscitation volumes? J Burn Care Rehabil 23:258, 2002; Cook RE et al: The role of angiography in the management
of haemorrhage from major fractures of the pelvis. J Bone Joint Surg Br 84:178, 2002; Dellinger RP et al: Surviving
Sepsis Campaign guidelines for management of severe sepsis and septic shock. Intensive Care Med 30:536, 2004;
Demling RH: The burn edema process: current concepts. J Burn Care Rehabil 26:207, 2005; Dente CJ et al: The outcome
of open pelvic fractures in the modern era. Am J Surg 190:830, 2005; Eastridge BJ et al: The importance of fracture
pattern in guiding therapeutic decision-making in patients with hemorrhagic shock and pelvic ring disruptions. J Trauma
53:446, 2002; Gurevitz S et al: The role of pelvic fractures in the course of treatment and outcome of trauma patients. Isr
Med Assoc J 7:623, 2005; Hemington-Gorse SJ: Colloid or crystalloid for resuscitation of major burns. J Wound Care
14:256, 2005; Inoue T et al: Effect of smoke inhalation injury on fluid requirement in burn resuscitation. Hiroshima J Med
Sci 51:1, 2002; Levy MM et al: 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Intensive
Care Med 29:530, 2003; Nguyen HB et al: Early goal-directed therapy, corticosteroid, and recombinant human activated
protein C for the treatment of severe sepsis and septic shock in the emergency department. Acad Emerg Med 13:109,
2006; O'Mara MS et al: A prospective, randomized evaluation of intra-abdominal pressures with crystalloid and colloid resuscitation
in burn patients. J Trauma 58:1011, 2005; Sheng Z: Prevention of multiple organ dysfunction syndrome in patients
with extensive deep burns. Chin J Traumatol 5:195, 2002; Starr AJ et al: Pelvic ring disruptions: prediction of
associated injuries, transfusion requirement, pelvic arteriography, complications, and mortality. J Orthop Trauma 16:553,
2002; Taeger G et al: Damage control orthopedics in patients with multiple injuries is effective, time saving, and safe. J
Trauma 59:409, 2005; van den Berghe G et al: Intensive insulin therapy in the critically ill patients. N Engl J Med
345:1359, 2001;
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial relationship
with the manufacturer or provider of any commercial product or service discussed. For this issue, the faculty reported
nothing to disclose.
Drs. Potenza, Schwartz, and Coimbra were recorded July 21, 2005, at Critical Care, sponsored by the University of
California, San Diego, School of Medicine. The Audio-Digest Foundation thanks the speakers and the University of
California, San Diego, School of Medicine for their cooperation in the production of this program.
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