CRITICAL CARE
| MANAGING THE TRAUMA PATIENT WHO ARRIVES WITH ANTICOAGULANTS ON BOARD —John T. Owings,
MD, Professor of Surgery and Chief of Surgical Critical Care, University of California, Davis, School of Medicine
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| Causes of bleeding: anticoagulant may not be cause; surgical causes—unligated vessel; ruptured spleen; bleeding from mesenteric
rent; others—temperature (cold patients prone to bleeding because cold acts as anticoagulant); liver dysfunction;
drugs
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| Severity of bleeding: location of bleeding determines severity; in abdomen, 2 L life-threatening; in brain, 2 mL life-threatening;
bleeding can manifest as drop in hematocrit or drop in mental status with stable hematocrit
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| Managing patients taking warfarin (Coumadin): Coumadin can cause moderate-to-severe bleeding and has predilection
for bleeding into brain; fresh frozen plasma—used to replete factors depleted by Coumadin; takes 6 to 8 hr to work
(due to time needed to order, thaw, administer, and realize effects); vitamin K—takes full day for effects to be seen; activated
coagulation factor VIIa—strong procoagulant; available at pharmacy; effects seen within minutes; effective for
patients who present with existing coagulation deficit; immediately corrects international normalized ratio (INR)
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| Managing patients taking low-molecular-weight heparin (LMWH): typically, heparin does not cause severe bleeding;
can cause severe bleeding in postoperative trauma patients; protamine effective in reversing effects of regular heparin;
for LMWH, generally have to wait 2 to 3 hr for drug to wear off before performing surgery (protamines specific to
each LMWH being developed)
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| Managing patients taking pentasaccharide: protamines not effective; pentasaccharide half-life 12 to 24 hr; patients taking
pentasaccharide do not tend to have severe bleeding associated with Coumadin or platelet inhibitors; requires judgment
in assessing risk of waiting to operate against risk of bleeding
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| Managing patients taking platelet inhibitors: aspirin—effects irreversible but cleared from circulation within 45 min;
platelet transfusion reverses defect; desmopressin (DDAVP) reverses aspirin effects by altering structure of platelets and
endothelium; clopidogrel (Plavix)—causes moderate-to-severe bleeding; irreversibly alters platelets; half-life 8 hr;
platelet transfusion ineffective because platelets inactivated by circulating drug; if waiting for drug to clear not an option,
take extreme care to prevent bleeding while operating; DDAVP and factor VIIa not effective
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| WHEN CAN YOU TRUST CT DIAGNOSIS OF PULMONARY EMBOLISM —John T. Anderson, MD, Associate Professor
of Surgery, University of California, Davis, School of Medicine
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| Diagnostic tools: pulmonary angiography—considered gold standard, but invasive and resource intensive; computed
tomography (CT) angiography—widely available and increasing in acceptance
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| Literature review: initial experience with CT artificially good because patients with indeterminate CT eliminated from
studies; in late 1990s, evidence showed procedure less effective; meta-analysis—12 studies comparing pulmonary angiography
to CT; CT sensitivity 74%, specificity 90%; CT utilized slices of 3-mm to 5-mm collimation and single detectors,
so new scanners likely give better results; study—comparison of CT to pulmonary angiography for detection of
subsegmental emboli (15% of patients with diagnosis of pulmonary embolism [PE] have only subsegmental clot); CT
sensitivity 46%; study—comparison of CT to pulmonary angiography for visualization of pulmonary blood vessels;
when looking at subsegmental areas, pulmonary angiography failed to show all vessels in 3.3% of cases; CT showed all
vessels in little over half of cases; study—subsegmental vessels not visualized by CT multidetector scanners in >20% of
cases
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| Predictive value of CT: use of CT likely to reduce number of patients with clinically suspected PE; positive predictive
value—analysis of studies involving patients with isolated clot detected on CT and suspected subsegmental PE shows
66% actually have PE; likely that only 10% of patients have PE when radiologist says CT shows isolated subsegmental
clot; negative predictive value—CT shown to have good negative predictive value
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| CT in intensive care unit (ICU): contrast dyes and timing altered by poor hemodynamics, so likelihood of false negatives
and false positives increases; study—for trauma, ICU, and intubated patients, CT sensitivity 40% and specificity 91%
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| Conclusions: CT that shows large central embolism in patient with suspected PE likely to be correct, so proceed with treatment;
pulmonary angiography required if CT indeterminate; speaker recommends pulmonary angiography in patient with
isolated subsegmental clot and high risk for anticoagulation; pulmonary angiography indicated for patients in ICU; CT
better than ventilation-perfusion (V/Q) scan
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| CYTOKINES YOU SHOULD KNOW —Lynette A. Scherer, MD, Assistant Professor of Surgery, University of California,
Davis, School of Medicine
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| Proinflammatory cytokines: tumor necrosis factor (TNF)-α—incites inflammation and initiates cytokine response; interleukin
(IL)-1—similar actions to TNF but not as vigorous; IL-6—has proinflammatory actions but also turns TNF
off; acts as surrogate for TNF response because longer lasting and easier to measure; others—chemokines activate neutrophils;
interferons; IL-2; colony stimulating factors
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| Anti-inflammatory cytokines: IL-10 tries to turn off cells producing TNF; IL-4; IL-13; transforming growth factor
(TGF)- β
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| Systemic actions of TNF: fever; acute-phase protein synthesis; cachexia; myocardial depression (important in septic patients);
disseminated intravascular coagulation (DIC; causes thrombosis in small capillaries of end organs); associated
with hypoglycemia
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| Interleukin-1: synergistic with TNF; incites fever; increases intracellular adhesion molecule (ICAM)-1 expression, which
causes activated white blood cells to stick to endothelial bed in area of inflammation; increases arachidonic acid metabolism
(substrate for prostaglandins and other inflammatory substances); induces somnolence; associated with anorexia
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| Cytokine cascade: any injury (eg, infection, toxins, injury, sepsis, surgery) activates macrophages that release IL-1, TNF,
and interferon (some organisms, particularly gram-negative organisms, have lipopolysaccharides [LPS] that directly
stimulate hypothalamus and induce fever); hypothalamic endothelium has specific receptors for TNF, IL-1, and LPS; hypothalamus
produces prostaglandin E2 when stimulated, which leads to increased cyclic adenosine monophosphate
(AMP) and, in turn, increased thermoregulatory set point, ie, fever; fever inhibition—prostaglandin E2 produced by cyclooxygenation
of arachidonic acid in cell membrane; cyclooxygenase inhibitors prevent prostaglandin E2 production
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| Cytokines and clinic experience: cytokines driving force behind systemic inflammatory response syndrome (SIRS),
acute respiratory distress syndrome (ARDS), and multiorgan system failure (MOSF); unable to control these disease
states with anticytokine therapy; activated protein C—speaker does not recommend use due to flawed studies; inhibits
clotting cascade, blocks cytokine cascade in proximal stages, and makes neutrophils less likely to stick to vascular endothelium;
anticytokine therapy for Crohn’s disease—infliximab (Remicade; chimeric protein) and adalimumab (Humira;
human protein) act as anti-TNF agents by binding to circulating and membrane-bound TNF, reducing
symptomatology
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| VENTILATOR-ASSOCIATED PNEUMONIA —Felix D. Battistella, MD, Professor of Surgery and Chief of Division of
Trauma surgery, University of California, Davis, School of Medicine
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| Background: pneumonia accounts for more than half of infections in critically ill patients; ventilator-associated pneumonia
(VAP) associated with significant mortality; pneumonia accounts for significant proportion of postoperative deaths
from infection; study—in 2 large series looking at VAP incidence per 1000 ventilator days, surgical patients had much
higher incidence than medical patients
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| Establishing diagnosis: Johanson criteria used widely (easy to apply but gives many false positives and negatives); more
invasive procedures advocated, eg, bronchoscopy with bronchoalveolar lavage or protected specimen brush samples
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| Delay in diagnosis: delay in establishing diagnosis increases morbidity and mortality; study—rate of pneumonia-related
sepsis higher if pneumonia occurs when patient on ventilator; study—24-hr delay in treating VAP led to increased mortality
and incidence of bacteremia
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| Treatment: Pugin et al, 1991—defined Clinical Pulmonary Infection Score (CPIS); series of parameters scored from 0 to
2; score >6 suggestive of pneumonia; study—antibiotics administered to patients with suspected pneumonia; CPIS taken
at initiation of therapy and 3 days later; of patients with CPIS <6 at initiation and 3-day follow-up, some continued on antibiotics
(standard course) and some had therapy withdrawn (short course); patients in standard-course group had higher
antibiotic resistance, longer ICU stays, and higher mortality rate; study—patients with pneumonia randomized to 1-wk
or 2-wk course of antibiotics; no difference in recurrence rate and incidence of mortality between groups; suggests patients
being treated longer than necessary; subgroup of patients with nonfermenting gram-negative bacilli (eg,
Pseudomonas) had higher recurrence rate
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| Treatment algorithm: if pneumonia suspected, calculate CPIS at initiation of antibiotics and 3-day follow-up; if CPIS >6,
treat patients with 1-wk antibiotic course (2-wk course for patients with Pseudomonas); if CPIS <6 at 3-day follow-up,
discontinue therapy
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| Prevention: minimize duration of ventilation—establish weaning protocol; daily interruption of sedation; prevent
aspiration—place head of bed at 30°; avoid gastric distention; Centers for Disease Control and Prevention (CDC)
recommendations—available at http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5303a1.htm
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| END POINTS OF RESUSCITATION —James W. Davis, MD, FACS, Associate Professor of Clinical Surgery, University
of California, San Francisco, School of Medicine, Fresno
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| Lactate and mortality: study—56 ICU patients in shock; 81% of patients with normal lactate survived; 90% of patients
with high lactate died; Vitek and Cowley study—of 126 patients in shock, survivors had lactate of 4.5 mEq/L, nonsurvivors
had levels of 8 mEq/L; lactate level at which 50% of patients died (LD50 ) 7.3 mEq/L; lactate normalized more
slowly in shock patients than in nonshock patients; lactate that did not normalize bad prognostic indicator; study—100%
of trauma patients survived if lactate cleared within first 24 hr, 70% if cleared in 24 to 48 hr, 11% if not cleared within 48
hr
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| Lactate and multiorgan system dysfunction (MOSD): initial and peak lactate levels and duration of hyperlactatemia
correlate with development of MOSD
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| Base deficit (BD): amount of fixed acid or base added to liter of blood to make pH 7.4 (calculated value); Weiskopf,
1982—base deficit has stoichiometric relationship to lactate; Davis, 1994—lactate and base deficit measured in porcine
hemorrhagic shock model; BD correlated well with arteriovenous O2 difference and mixed and central venous O2 saturation;
as lactate increased, BD decreased
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| Base deficit and trauma: study—in 66 battle casualties, BD present in patients with shock and normal pH; Davis et
al—in 209 civilian trauma patients, BD associated with lower blood pressure (BP) and greater volume of resuscitation;
overall—admission BD correlates with BP, injury severity score, trauma score, need for transfusion, development of
ARDS and MOSF, IL-6 and CD11b levels, and mortality
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| Base deficit and transfusion: study—of patients with normal BD, 11% transfused; if BD <-6, 72% transfused
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| Base deficit and mortality: of patients with normal BD, 6% die; mortality increases with increasing BD; mortality increases
as time from admission to normalization of BD increases
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| Confounders of metabolic indices: ethanol; methamphetamines and cocaine; seizures; aspirin; Champion, 1993—pH
confounded by ethanol, so BD probably more useful; Dunne et al, 2002—21% of trauma patients had alcohol in system;
7% had other drugs; BD and lactate valuable as predictors of outcome; Davis et al—BD <-6 predictive of significant
injury and need for transfusion; transfusion requirement dropped from >70% to 60% when patient intoxicated
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| Lactate vs base deficit: study—in resuscitated ICU patients, lactate correlated with mortality, BD and anion gap did not;
Kincaid et al—100 patients in ICU with pulmonary artery catheters and normal lactates; patients with persistent BD had
higher incidence of multiorgan failure and mortality, and BD correlated with O2 consumption and utilization
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| Physical examination: study—2 intensivists examined all patients diagnosed with hypoperfusion to determine whether
patient clinically hypoperfused (warm vs cool); cool and clammy patients had lower cardiac index, pH, and bicarbonate
and higher lactate
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| Gastric tonometry: becoming less popular; based on theory that subclinical ischemia can be detected in splanchnic bed;
increased tissue PCO 2 and decreased tissue pH disrupts gastric mucosa; gap between intragastric PCO 2 and arterial PCO 2
correlates to degree of ischemia; need to withhold feedings and suppress acid secretion; correlates with MOSD syndrome,
mortality if pH <7.32, lactate, and BD
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| Sublingual PCO 2 : correlates with lactate, presence of shock, and survival; in studies using probes inserted into muscle to
measure tissue O2 , patients with higher PCO 2 and lower O2 had increased mortality; potential confounders include hypothermia
and vasoconstriction
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| Near infrared spectroscopy (NIRS): determines redox state of light-absorbing molecules (hemoglobin, myoglobin, and
cytochrome aa3 change their spectra when oxygenated); indicative of venous oxyhemoglobin desaturation; studies—
cerebral cortex and calf muscle O2 decreased in proportion to blood loss; better at gauging ongoing resuscitation; aids in
diagnosis of compartment syndrome
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Educational Objectives
| The goal of this program is to educate the listener about issues in critical care. After hearing and assimilating this program,
the clinician will be better able to:
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 | 1. Manage trauma patients taking anticoagulant medication.
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| 2. Utilize computed tomography in the diagnosis of pulmonary embolism.
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| 3. Review the cytokine response to trauma.
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| 4. Diagnose and treat ventilator-associated pneumonia.
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| 5. Discuss the use of lactate and base deficit as end points of resuscitation in trauma patients.
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Discussed on This Program
Adalimumab [Humira]
Aspirin (acetylsalicylic acid; ASA) [several trade names]
Clopidogrel bisulfate [Plavix]
Coagulation factor VIIa (recombinant) [NovoSeven]
Desmopressin acetate (1-deamino-8-D-arginine vasopressin) [DDAVP, Stimate]
Heparin sodium injection
Infliximab [Remicade]
Warfarin sodium [Coumadin]
Suggested Reading
Anderson JT et al: Diagnosis of posttraumatic pulmonary embolism: is chest computed tomographic angiography acceptable?
J Trauma 54(3):472, 2003; Ashare A et al: Anti-inflammatory response is associated with mortality and severity of
infection in sepsis. Am J Physiol Lung Cell Mol Physiol 288(4):L633, 2005; Baron BJ et al: Diagnostic utility of sublingual
PCO2 for detecting hemorrhage in penetrating trauma patients. J Trauma 57(1):69, 2004; Chastre J et al: Comparison
of 8 vs 15 days of antibiotic therapy for ventilator-associated pneumonia in adults: a randomized trial. JAMA
290(19):2588, 2003; Dunham CM et al: Base deficit level indicating major injury is increased with ethanol. J Emerg Med
18(2):165, 2000; Dunn AS et al: Perioperative management of patients on oral anticoagulants: a decision analysis. Med
Decis Making 25(4):387, 2005; Iregui M et al: Clinical importance of delays in the initiation of appropriate antibiotic
treatment for ventilator-associated pneumonia. Chest 122(1):262, 2002; Kaplan LJ, Kellum JA: Initial pH, base deficit,
lactate, anion gap, strong ion difference, and strong ion gap predict outcome from major vascular injury. Crit Care Med
32(5):1120, 2004; Larson BJ et al: A feasibility study of continuing dose-reduced warfarin for invasive procedures in patients
with high thromboembolic risk. Chest 127(3):922, 2005; Lighthall GK et al: Correction of intraoperative coagulopathy
in a patient with neurofibromatosis type I with intravenous desmopressin (DDAVP). Int J Obstet Anesth 13(3):174,
2004; Marelich GP et al: Protocol weaning of mechanical ventilation in medical and surgical patients by respiratory care
practitioners and nurses: effect on weaning time and incidence of ventilator-associated pneumonia. Chest 118(2):459,
2000; Minei JP et al: Alternative case definitions of ventilator-associated pneumonia identify different patients in a surgical
intensive care unit. Shock 14(3):331, 2000; Narong MN et al: Surgical site infections in patients undergoing major operations
in a university hospital: using standardized infection ratio as a benchmarking tool. Am J Infect Control 31(5):274,
2003; Nguyen NT et al: Systemic coagulation and fibrinolysis after laparoscopic and open gastric bypass. Arch Surg
136(8):909, 2001; Perrier A et al: Multidetector-row computed tomography in suspected pulmonary embolism. N Engl J
Med 352(17):1760, 2005; Schoepf UJ: Computed tomography for pulmonary embolism diagnosis: the making of a reference
standard. J Thromb Haemost 3(9):1924, 2005; Tillie-Leblond I et al: Risk of pulmonary embolism after a negative
spiral CT angiogram in patients with pulmonary disease: 1-year clinical follow-up study. Radiology 223(2):461, 2002;
Tisherman SA et al: Clinical practice guideline: endpoints of resuscitation. J Trauma 57(4):898, 2004; Varkarakis IM
et al: Laparoscopic renal-adrenal surgery in patients on oral anticoagulant therapy. J Urol 174(3):1020, 2005; Velmahos
GC et al: Spiral computed tomography for the diagnosis of pulmonary embolism in critically ill surgical patients: a comparison
with pulmonary angiography. Arch Surg 136(5):505, 2001; Zehtabchi S et al: Ethanol and illicit drugs do not affect
the diagnostic utility of base deficit and lactate in differentiating minor from major injury in trauma patients. Acad
Emerg Med 11(10):1014, 2004;
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 following
has been disclosed: Dr. Davis is a member of the Speakers’ Bureau of KCI and Novartis.
Drs. Owings, Anderson, Scherer, and Battistella were recorded September 17-19, 2004, at General Surgery 2004—26th
Annual Postgraduate Course sponsored by the University of California, Davis, Health System, and held in Olympic Valley,
California. Dr. Davis was recorded January 29th , 2005, at the 33rd Annual Phoenix Surgical Symposium sponsored by
the Maricopa Integrated Health System and the Phoenix Surgical Society and held in Scottsdale, Arizona. The Audio-Digest
Foundation thanks the speakers and the sponsors for their cooperation in the production of this program.
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