TRAUMA OF SOLID ORGANS
| PUSHING THE NONOPERATIVE ENVELOPE IN HEPATIC TRAUMA —John A. Weigelt, MD, Milt Lunda Professor
of Surgery, Medical College of Wisconsin, Milwaukee
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| Principles of nonoperative management (NOM) of hepatic trauma: blunt mechanism of injury; hemodynamic
normality (or resuscitation from shock to period of hemodynamic normality); injury graded by computed tomography
(CT); resuscitation protocol and availability of surgeon; American Association for the Surgery of Trauma
(AAST) grading system most useful in categorizing types of injuries (and in studying outcomes that occur with different
injuries), but not very useful in day-to-day management of patients
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| Injury mortality and success rate of NOM: since 1980s, mortality rates for blunt hepatic injuries have declined
dramatically, as practice of NOM has increased; limited data on NOM of penetrating liver trauma (speaker suggests
NOM not appropriate for these injuries); currently, 85% to 90% of all blunt liver injuries managed nonoperatively;
overall success rate of NOM 85% to 100%, depending on grade of injury (as grade increases, success decreases)
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| Role of angiography and embolization: drive for earlier use of angiography and embolization as way to “push the
envelope” in NOM of hepatic trauma; however, according to review of recent data (University of Louisville study;
study by Mohr et al [450 patients with grade 3 to 5 blunt liver injuries]; study by Kozar et al), unclear whether this approach
increases success rate of NOM; from speaker’s experience, increasing incidence of complications (eg, liver necrosis)
becoming apparent as more patients undergo early embolization for reasons related only to CT grading of
injury
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| Recommended role for angiography and embolization: best candidate—hemodynamically normal; isolated
liver injury; blush on CT, but continues to require fluid resuscitation (and has no other source of blood loss); do not
want to invade these patients operatively, and angioembolization may be helpful; early intervention promoted in those
with grade 4 or 5 injury, or large amount of intraperitoneal blood with blush on CT, despite hemodynamic normality
(data unclear whether helpful in these cases); routine early use in hemodynamically normal patients, based solely on
grade of injury or amount of intraperitoneal blood “unwise at this time”
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| Conclusions: NOM standard treatment for blunt liver injuries; hemdoynamic status drives decision making, not CT
grade of injury; surgical intervention remains viable option; angiographic complications real, and procedure should not
be routine in severe liver injuries; speaker believes this represents “pushing the envelope” (using technology where inappropriate);
recommended protocol —1) with blunt hepatic injury when hemodynamics normal, patient enters nonoperative
schema; most admitted and observed, do activities of daily living, and discharged within 3 to 4 days; 2) in some,
especially those with grades 3 and 4 injuries, complications may develop (eg, bilomas, hepatic abscesses), which need to
be drained; 3) occasionally, patients develop hemodynamic abnormalities while being observed; angiography useful in
these cases (especially as one follows hemodynamics, not CT); 4) patient admitted with abnormal hemodynamics requires
early surgery, and angiography can be used as adjunct postoperatively
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| PUSHING THE NONOPERATIVE ENVELOPE IN SPLENIC TRAUMA —Dr. Weigelt
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| Indications for nonoperative management (NOM) of splenic trauma: blunt mechanism of injury; hemodynamic
normality; injury diagnosed by CT (usually related to no other abdominal injuries; extra-abdominal injuries can
be present); guideline helpful to drive NOM approach
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| Hemodynamic normality: responder to fluid resuscitation usually patient with no more than class II shock; in case
of splenic injury, preferable to not transfuse patients if possible; some centers allow blood transfusion limit of 2.0 U
for adult with splenic injury only; however, in patients with additional injuries, criteria for blood transfusion should be
based on those injuries
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| Role of guideline in driving results and outcomes of NOM: in 1999, speaker’s institution established guideline
that hemodynamically normal patients with blunt splenic injury should enter NOM; comparison of patient outcomes before
and after establishment of guideline show decrease in splenectomy rate from 41% to 23%; before guideline, splenic
salvage rate estimated to be 65%; in 2004, most published reports showed salvage rates of 85%, once institution started
NOM guideline
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| Benefits of NOM: clearly demonstrated in literature; preservation of splenic function; less transfusion for splenic injury;
less morbidity; shorter length of stay; reduced cost
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| Angioembolization: currently touted for increased use in treatment of splenic injuries; current indications include
contrast blush seen on CT, or “just a splenic injury”; 3 types of blush identified (contained intraparenchymal blush;
blush localized to spleen and surrounding tissues; intraperitoneal bleeding from blush [these patients usually hemodynamically
abnormal]); speaker suggests that angioembolization based merely on presence of splenic injury not appropriate;
first 2 types of blush commonly associated with hemodynamic normality and infrequently progress to point
where splenectomy needed; most of these patients undergo successful NOM
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| Possible benefits and effects of angioembolization: on preservation of splenic function —2 recent studies suggest
no substantial reduction in mortality; on immune function— function best when patient has intact artery and 50%
of splenic mass; in literature, after embolization of spleen, infarction rate 25%; no data on whether spleens immunologically
competent after infarction; on resource use—greater transfusion rate and greater length of hospital stay; on
splenic salvage—study showed overall salvage rate with embolization 82%; most studies of NOM without embolization
showed overall rate of 85%
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| Complications associated with angioembolization: pleural effusions common after embolization of any portion
of spleen (can produce substantial morbidity in patients with associated rib fractures or pulmonary contusions); in recent
study, complications relevant to angiographic intervention included continued bleeding, missed injuries, infection
in left upper quadrant, and vascular injury
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| Retrospective review of patients who failed NOM (Peitzman et al): 25% of these patients in shock (ie, hemodynamically
abnormal); diagnostic mistakes made in 19 cases (misread CT and false-negative focused abdominal
sonographic examinations); 10 patients died; in retrospect, 30% to 40% inappropriate candidates for NOM
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| Conclusions: currently, NOM 85% successful in properly selected patients (speaker suggests approaching 95% if patients
selected appropriately and current information from literature followed); routine angiography for simple contrast
blush by CT or for presence of splenic injury “pushing the envelope” too far (reported negative effects of angiography include
increases in transfusions, complications, length of stay, and cost; also unknown effects on splenic function and
mortality); currently, can safely proceed with NOM in majority of patients with blunt splenic injury who are hemodynamically
normal; angiography may be useful in extremely small number of patients; routine use inappropriate
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| PANCREATIC TRAUMA —Michael D. McGonigal, MD, Assistant Professor, Department of Surgery, University of
Minnesota Medical School, Minneapolis, and Director, Trauma Services, Regions Hospital, St. Paul, MN
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| Mechanisms of injury: penetrating or blunt; penetrating injury “very straightforward”; majority of cases blunt
trauma; however, much more difficult to hurt pancreas through blunt injury (requires direct anterior blow to epigastrium);
most commonly seen in assault victims, patients with handlebar injuries, and deceleration injuries
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| Early indications: vague; abdominal pain—impossible to differentiate from pain caused by other abdominal injuries,
and pancreatic injury almost never isolated event; progression insidious if missed initially; systemic response—eg, unexplained
fever, rise in white blood cell (WBC) count more immediately apparent than clinical response; unfortunately, this
rise frequently masked by systemic response to trauma and other injuries; abnormal CT—probably most reliable indicator,
but “still unreliable”
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| Critical decision points: hemodynamic instability; findings of peritonitis; evidence of pancreatic injury on CT; other
significant injuries requiring surgery; patient’s intraoperative hemodynamics, temperature, and coagulation status
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| Diagnostic methods: CT (useful only if patient hemodynamically stable and does not have peritoneal findings);
endoscopic retrograde cholangiopancreatography (ERCP; can be useful in providing additional information when CT
findings suspicious; however, requires skilled endoscopist); direct examination with scapel
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| Tips and tricks for duct examination: probably most important aspect of assessing injured pancreas determining
whether ductal disruption present, and, if so, extent of injury; most direct method simple debridement of injured area
and direct inspection; other options include pancreatography (distal [classic textbook approach] or proximal), and intraoperative
ERCP (“usually an exercise in futility”)
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| Operative management options: debridement with drainage most common approach (appropriate for patients with
no ductal injury or those with minor ductal injuries); consider distal pancreatectomy in patients with more complicated
problem; splenic salvage not appropriate in most cases of surgery for pancreatic trauma; if damage to right side of superior
mesenteric vein, or combined pancreaticoduodenal injuries, Whipple procedure may be necessary; duodenum
should always be closely inspected (because duodenum and pancreas so close to each other, difficult to imagine one
being injured without the other, especially when dealing with blunt trauma)
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| General operative principles: perform thorough intraoperative evaluation (must inspect pancreas from every direction
possible; open lesser sac; inspect entire duodenum); keep it simple (debridement and drainage key components of
dealing with pancreatic trauma; avoid complex reconstructions if possible); in cases requiring more complicated procedure
(eg, total pancreatectomy or Whipple procedure), seriously consider damage control surgery (these patients do
not tolerate lengthy procedures)
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| Damage control in pancreatic trauma: usual principles apply, ie, control hemorrhage and contamination; continually
reassess patient status
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| Recommendations: always suspect pancreatic or duodenal injury in patient with appropriate mechanism or with suspicious
findings on CT; preoperative evaluation performed only on patients with no findings of peritonitis and who
have normal vital signs; thorough intraoperative examination key; always consider damage control; never perform total
or near total pancreatectomy during first laparotomy
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| SEDATION: HOW TO GET IT JUST RIGHT —Edward E. Cornwell III, MD, Professor of Surgery, and Chief, Adult
Trauma Service, Johns Hopkins University School of Medicine, Baltimore, MD
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| Introduction: critical care patients injured and agitated; patients in intensive care unit (ICU) can progress easily from
agitation to anxiety, fear, distress, and in some cases, disorientation, hallucination, and loss of personal control; goals
of sedation patient comfort and amnesia of traumatic events; adequate pain control also important prerequisite
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| Delirium: most common psychiatric syndrome in general hospital setting; symptoms—extreme excitement; impaired
memory, rapid succession of confused unconnected ideas; proposed mechanism—derangement in central cholinergic
efficiency; triggers—metabolic derangements; infectious processes; medications; risk factors—male sex; advanced
age; fever; history of ethanol abuse
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| End points of sedation: communicated through Ramsay sedation scale; frequently, goal cooperative patient who accepts
mechanical ventilation, yet still follows commands; physicians and nursing staff not always in agreement on end
points of therapy
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| Indications for specific drugs: pain (analgesic); anxiety (benzodiazepines); extreme agitation (sedative hypnotics);
delusions, hallucinations, and delirium (neuroleptics and antipsychotics)
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| Benzodiazepines: midazolam (Versed), lorazepam (eg, Ativan), diazepam (eg, Valium); speaker uses midazolam in
patients who require short-term sedation (only one of these 3 agents with short enough half-life to allow use in continuous
drip; lorazepam and diazepam have longer half-lives and tend to be used as q8h to q12h drugs); based on patient’s
agitation and length of sedation required, give 1 mg midazolam (if simply required for procedure), or 1 mg
lorazepam, if possible hepatic dysfunction (lorazepam metabolized by conjugation; midazolam and diazepam metabolized
by hepatic oxidation)
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| Longer-term sedation: speaker prefers propofol in several settings; dosing regimen differs, depending on goals of
therapy; “we intensivists tend to give it to patients who are intubated” (propofol profound respiratory depressant when given
in doses high enough to produce unconsciousness); eg, speaker uses propofol for bedside percutaneous tracheostomies;
many gastroenterologists use propofol in lower doses in outpatient setting without intubating patients; propofol expensive
but easily titrated based on its short onset of action
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| Extreme delirium and possible psychosis and delusions: speaker recommends haloperidol (Haldol); decreases
patient’s responsiveness to external stimuli but does not change his or her awake state and does not affect intellect;
dosing regimen function of patient’s age and level of agitation; start with 2.0 to 2.5 mg/kg and increase as necessary
every 20 to 30 min; then calculate number of milligrams used to achieve desired level of sedation, and give same
amount over next 24 hr; if successful, start to wean patient off drug over next several days
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| Case scenarios: control of pain and agitation in ICU; patient with single stab wound to chest who requires placement of
chest tube; patient with blunt trauma requiring extended diagnostic work-up before admission, or patient requiring long-
term sedation for extended postsurgical stay in ICU; treatment of open abdominal wound; “doctor in charge” syndrome
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| Conclusion: task of getting sedation right involves science of pharmacotherapy with sedatives and hypnotic agents
and art of matching agents to individual patient scenarios
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Suggested Reading
Brasel KJ et al: Splenic injury: trends in evaluation and management. J Trauma 44:283, 1998; Carillo EH et al: Interventional
techniques are useful adjuncts in nonoperative management of hepatic injuries. J Trauma 46:619, 1999; Cerwenka
H et al: Management of pancreatic trauma and its consequences--guidelines or individual therapy?
Hepatogastroenterology 54:581, 2007; Chrysos E et al: Pancreatic trauma in the adult: current knowledge in diagnosis
and management. Pancreatology 2:365, 2002; Cooney R et al: Limitations of splenic angioembolization in treating blunt
splenic injury. J Trauma 59:926, 2005; Crystal CS et al: Anesthetic and procedural sedation techniques for wound management.
Emerg Med Clin North Am 25:41, 2007; Dent D et al: Blunt splenic injuries: high nonoperative management
rate can be achieved with selective embolization. J Trauma 56:1063, 2004; Ekeh AP et al: Complications arising from
splenic embolization after blunt splenic trauma. Am J Surg 189:335, 2005; Fata P et al: A survey of EAST member practices
in blunt splenic injury: a description of current trends and opportunities for improvement. J Trauma 59:836, 2005;
Haan JM et al: Splenic embolization revisited: a multicenter review. J Trauma 56:542, 2004; Kao LS et al: Predictors
of morbidity after traumatic pancreatic injury. J Trauma 55:898, 2003; Koniaris LG: Role of pancreatectomy after severe
pancreaticoduodenal trauma. J Am Coll Surg 198:677, 2004; Kozar RA et al: Complications of nonoperative management
of high-grade blunt hepatic injuries. J Trauma 59: 1066, 2005; Lin BC et al: Management of blunt major pancreatic
injury. J Trauma 56:774, 2004; Lopez PP et al: Blunt duodenal and pancreatic trauma. J Trauma 53:1195, 2002; Mohr
AM et al: Angiographic embolization for liver injuries: low mortality, high morbidity. J Trauma 55:1077, 2003; Peitzman
AB et al: Failure of observation of blunt splenic injury in adults: variability in practice and adverse consequences. J
Am Coll Surg 201:179, 2005; Phelan HA, Minei JP: Pancreatic trauma: diagnostic and therapeutic strategies. Curr
Treat Options Gastroenterol 8:355, 2005; Richardson JD: Changes in the management of injuries to the liver and
spleen. J Am Coll Surg 200:648, 2005; Rickard MJ et al: Pancreatic and duodenal injuries: keep it simple. ANZ J Surg
75:581, 2005; Sclafani SJ et al: Nonoperative salvage of computed tomography-diagnosed splenic injuries: utilization of
angiography for triage and embolization for hemostasis. J Trauma 39:818, 1995; Wahl WL et al: The need for early angiographic
embolization in blunt liver injuries. J Trauma 52:1097, 2002; Zhang SH et al: Diagnosis and treatment of pancreatic
trauma. Chin J Traumatol 8:303, 2005.
Educational Objectives
| The goal of this program is to improve management of solid organ trauma. After hearing and assimilating this program,
the clinician will be better able to:
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 | 1. Explain the indications for and benefits of nonoperative management (NOM) of hepatic and splenic trauma.
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| 2. Take into account recent data on the effects and complications of angioembolization when considering this intervention
as an adjunct to NOM.
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| 3. Describe the mechanisms of injury for pancreatic trauma and the diagnostic methods used to assess the injury.
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| 4. Recall the recommended operative approaches to pancreatic trauma and discuss the importance of damage control
surgery in these patients.
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| 5. Achieve the best and most effective level of sedation by matching specific sedatives and hypnotic agents to individual
patient scenarios.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty members 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 reported nothing to disclose.
Acknowledgements
Drs. Weigelt and McGonigal spoke at Advances in Hepatic, Biliary, and Pancreatic Surgery, held June 14-17, 2006,
in Minneapolis and sponsored by the University of Minnesota, Minneapolis, Medical School. Dr. Cornwell lectured
at the 13th Annual USC Trauma/Critical Care Symposium, held May 22-23, 2006, in Pasadena, CA, and sponsored
by the Keck School of Medicine of the University of Southern California, Los Angeles. The Audio-Digest Foundation
thanks the speakers and the sponsors for their cooperation in the production of this program.
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