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EMS NAVIGATOR
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SPRING 2012
For emergency medicine
and trauma professionals
In This Issue
1 Necrotizing Soft Tissue Infections
2 Lactate Helps to Improve Prehospital Triage
7 Calendar of Events
TRAUMA
8 EMS Navigator
Necrotizing Soft Tissue Infections
by Gina M. Howell, MD, and Matthew R. Rosengart, MD, MPH
Necrotizing soft tissue infections (NSTIs) are infrequent but aggressive and rapidly
spreading infections with potential for high morbidity and mortality. Though commonly
called necrotizing fasciitis, this name refers only to a subset of NTSIs that invade the
fascial layers. The basic pathophysiology involves the invasion and subsequent spread
of bacteria into the subcutaneous tissue, where they release enzymes and toxins
causing local tissue ischemia and necrosis. Associated stimulation of the production of
inflammatory cytokines promotes systemic toxicity, shock, multisystem organ
dysfunction, and death.
The incidence of NSTI is approximately 500-1500 cases per year in the United States
and is on the rise.1 Despite advances in medical care, mortality from NSTI remains as
high as 35 percent.2 Early surgical debridement constitutes the mainstay of treatment,
and has been shown in numerous studies to be the major determinant of survival. 3-6
Microbiology
Three basic microbial subtypes of NSTI are described. Type I, or polymicrobial, NSTI
is the most common form of disease, constituting 55 to 75 percent of all NSTI.4, 7-9
These infections tend to occur in the perineal and trunk region, and are often diagnosed
in patients with known risk factors or immune compromise. Type II infections are
monomicrobial infections caused by Group A Streptococcus (GAS), either alone or in
association with Staphylococcus aureus, and as such can be associated with toxic shock
syndrome. Despite its notoriety in the lay press as “flesh-eating” bacteria, Type II
infections are a much less common form of NSTI. These infections classically occur on
the extremities, and are more likely to be diagnosed in otherwise young, healthy hosts.
GAS can be an especially virulent pathogen, causing rapidly progressive disease due to
a variety of unique virulence factors.10,11
Type III NSTI, also known as myonecrosis or “gas gangrene,” is primarily caused by
Clostridium perfringens, and is much less common than types I or II NTSIs.
An emerging cause of NSTI is community-acquired methicillin-resistant S. aureus
(CA-MRSA), which is present in cultures of one-quarter to one-third of cases of NTSI.
This has important implications in the antibiotic management of NSTI, because many
of the recommended antibiotic regimens may not provide adequate coverage for MRSA.
(Continued on page 4)
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TR AUMA RO U NDS
Lactate Helps to Improve Prehospital Triage
by Francis X. Guyette, MD
The Problem
Shock has been defined by the American College of Surgeons as “the
presence of inadequate tissue perfusion and oxygenation” and, better still,
by Gross as “the rude unhinging of the machinery of life.” Prehospital
triage helps us to identify patients in shock who need of lifesaving
interventions (LSIs) — tasks done in the field or hospital to prevent
death. LSIs may include prehospital hemorrhage control, airway
management, or fluid resuscitation. In addition, once the patient is
brought to an emergency department, further action may be necessary
to prevent death, including emergent operation, resuscitation with fluid
or blood products, or definitive airway management. As prehospital
providers, our role is to identify those patients who need LSIs and
determine how to get them to the best care available.
when their vital signs are normal.7,8 A new generation of handheld,
point-of-care (POC) lactate analyzers is now available for use in EMS.
They work much like a standard glucometer..9
Importance
High lactate identifies patients who have a higher risk of death, need for
surgery, need for blood transfusions, and rate of ICU admission following
ED presentation. Lactate may be added to vital signs and mechanism of
injury to develop better triage criteria for trauma patients. In the near
future, lactate levels may help direct transport to regionalized trauma
centers for more aggressive early resuscitation. Ultimately, prehospital
protocols might use lactate to determine who might benefit from
treatment with fluids or medications.
Traditional trauma triage depends on vital signs and mechanism of injury,
which often do not predict need for LSIs or injury severity.1,2 Mechanisms
of injury are not accurate, and tend to send many uninjured people to the
hospital while adding little benefit. A recent study suggests that a high
heart rate (HR) and field hypotension (systolic blood pressure õ 90 mmHg)
predicts an increased risk of death but may miss many serious injuries. 3,4,5
Blood pressure and heart rate may change late in shock, and only when
the body can no longer compensate for blood loss. Furthermore, patients
with head injuries, the very old or very young, and those being treated
with certain medications (for example, beta blockers) may not exhibit
hypotension or tachycardia in response to traumatic injury.
Experience from Iraq and Afghanistan has taught us that very fit persons
may be able to keep near normal heart rates and blood pressures despite
life-threatening injuries. This type of “compensated shock” is not easily
recognized, and may lead to triage of some patients away from specialized
trauma centers and delayed resuscitation, which is strongly associated
with death.3,4,5
If paramedics cannot rely on mechanism of injury and vital signs, what
other tools can help them to identify shock in trauma patients? One
answer may be lactic acid, or lactate. Serum lactate is a byproduct of
anaerobic metabolism; we have all felt that our muscles “burn” after hard
exercise. Lactate is a circulating biomarker of poor organ oxygen supply
or high demand, and is directly related to death in patients with sepsis,
myocardial infarction, and trauma.6,7 Following lactate levels can help us
to identify patients who are not getting enough oxygen to tissues, even
Lactate meter.
The Evidence
Previous studies have demonstrated that lactate can predict severe
bleeding after trauma and is associated with need for hospital admission,
ICU admission, emergent intervention, and death.10,11 Trauma surgeons
at the University of Alabama, Birmingham, note that standard blood
pressure and heart rate monitoring underestimate the severity of
hemorrhage. Among patients with systolic blood pressure under
110 mmHg, an increase in lactate was associated with the need for
massive transfusion (more than six units of blood). They showed that
lactate was better than blood pressure alone for the identification of shock.
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In another study, trauma patients with high prehospital lactate were
more likely get admitted to the hospital and twice as likely to die even
when their vital signs were normal.12 The authors concluded that lactate is
better than all prehospital vital signs for the prediction of death and need
for hospital admission.13
References
Point-of-care lactate also has been used in a large air medical system
to identify shock.11,14 In this study, 400 trauma patients underwent
continuous vital sign monitoring and both prehospital and emergency
department lactate sampling. Those patients with prehospital lactate
levels >4 mmol/L had greater need for emergent operation, intubation,
and vasopressors. Lactate better predicted death and surgery even when
age, GCS, and initial vital signs were taken into account.14 Among the 265
3. Lipsky AM, Gausche-Hill M, Henneman PL, et al. (2000) “Prehospital
hypotension is a predictor of the need for an emergent, therapeutic
operation in trauma patients with normal systolic blood pressure in the
emergency department.” J Trauma 65(5):1228-1233.
patients with normal vital signs, those with lactates >4 mmol/L were five
times as likely to need surgery (odds ratio [OR] 5, confidence interval [CI]
1.5–16.2) and 3.5 times as likely to die (OR 3.5, CI 1.3–9.7) compared with
those with a lactate <4 mmol/L. Prehospital lactate strongly predicts
death and the need for emergent surgery among trauma patients with
normal vital signs.11,14
The Next Step
Although lactate is better than vital signs alone for identifying critical
trauma patients, we do not know if it is better than the overall result of
current paramedic triage (vitals, mechanism, and gut feeling). EMS
services in western Pennsylvania are part of a large multicenter study to
evaluate the ability of prehospital lactate to triage patients that could not
be otherwise identified by abnormal vital signs. In addition, a combination
of lactate and vital-sign criteria may give advance warning in patients
with life threatening hemorrhage. Lactate also may identify patients with
more severe conditions who could potentially benefit from lifesaving
interventions and new treatments.
Francis X. Guyette, MD, is an assistant professor of emergency
medicine, University of Pittsburgh School of Medicine, and associate
medical director, STAT MedEvac.
1. McGee S, Abernethy WB 3rd, Simel DL (1999) “The rational clinical
examination: is this patient hypovolemic?” JAMA 281(11):1022-1029.
2. Brasel KJ, Guse C, Gentilello LM, et al. (2007) “Heart rate: is it truly a
vital sign?” J Trauma 62(4):812-817.
4. Claridge JA, Crabtree TD, Pelletier SJ, et al. (2000) “Persistent occult
hypoperfusion is associated with a significant increase in infection rate
and mortality in major trauma patients.” J Trauma 48(1):8-14;
discussion 14-15.
5. Crowl AC, Young JS, Kahler DM, et al. (2000) “Occult hypoperfusion
is associated with increased morbidity in patients undergoing early
femur fracture fixation.” J Trauma 48(2):260-267.
6. Shapiro NI, Howell MD, Talmor D, et al. (2005) “Serum lactate as a
predictor of mortality in emergency department patients with
infection.” Ann Emerg Med 45(5):524-528.
7. Jansen TC, van Bommel J, Mulder PG, et al. (2008) “The prognostic
value of blood lactate levels relative to that of vital signs in the
pre-hospital setting: A pilot study.” Crit Care 12(6):R160.
8. Abramson D, Scalea TM, Hitchcock R, et al. (1993) “Lactate clearance
and survival following injury.” J Trauma 35:584-588.
9. Asimos AW, Gibbs MA, Marx JA, et al. (2000) “Value of point-of-care
blood testing in emergent trauma management.” J Trauma 48:11011108.
10. Vandromme M (2010) “Lactate is a better predictor than systolic
blood pressure for determining blood requirement and mortality: Could
prehospital measures improve trauma triage?” J Am Coll Surgeons
[Trauma] 210(5):861-867.
11. Guyette F (2009) “Identification of occult shock using out-of-hospital
lactate.” Ann Emerg Med 54(3):S142.
12. Gunnerson KJ (2008) “Prehospital lactate levels are better predictors
of mortality and hospital admission than traditional vital signs.”
Circulation 120(S):S1459.
13. Gunnerson KJ (2008) “Prehospital point of care lactate does not
correlate with initial hemodynamic variables.” Chest [Abstract]
138(Oct.):65003.
14. Castillo. (2009) “The role of prehospital lactate as a predictor of
outcomes in trauma patients.” J Trauma [Abstract].
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4
TR AUMA RO U NDS
(Continued from page 1)
Diagnosis
cases, the diagnosis of NTSI is best made on the basis of clinical
The diagnosis of NTSI is often delayed due to the lack of
exam and findings at surgical debridement.
recognition and the paucity of early clinical findings. One should
utilize a high index of suspicion and maintain a low threshold
for operative intervention in cases of suspected NSTI. This is
particularly relevant in managing patients with known risk factors:
diabetes mellitus, intravenous drug use, HIV, obesity, ethanol
Treatment
Rapid and simultaneous resuscitation, operative debridement,
and antibiotics are critical. Most patients with NTSI should be
rapidly triaged to a tertiary care center.
abuse, and recent trauma or surgery.12 However, a significant
number of NSTIs occur in otherwise healthy, immunocompetent
patients without these risk factors.
Table 2: The Laboratory Risk Indicator for Necrotizing Fasciitis
(LRINEC) Score
Variable
Partial Score
Clinical findings suggestive of NSTI include pain out of proportion
to exam, tense edema, ecchymoses, bullae, crepitus, local
C-reactive protein (mg/L)
anesthesia, systemic toxicity, and disease progression despite
<150
0
antibiotic therapy.13 Radiographic imaging in the form of plain film,
>150
4
CT, or MRI may reveal soft tissue gas, enhancement or thickening
of involved fascia, and/or associated abscesses.14 However, soft
WBC (cells/mm3)
tissue gas may be absent on x-ray in two-thirds of patients and on
<15
0
CT in a quarter of patients with documented NTSI; thus the
15-25
1
>25
2
absence of gas on imaging does NOT exclude the diagnosis of
NTSI. Furthermore, surgical consultation and treatment should
NOT be delayed in order to obtain imaging such as MRI. In many
Table 1: Group A Streptococcus Virulence Factors
Hemoglobin (g/dL)
>13.5
0
11-13.5
1
2
Virulence Factor
Function
<11
M protein
Surface proteins. Facilitate attachment to
host cells, inhibit phagocytosis. M1 and
M3 are most virulent subtypes.
Sodium (mmol/L)
Streptolysin O, S
Beta-hemolysis.
Streptokinase
Activates plasminogen.
Exotoxins
Damages endothelium, causes loss
of microvascular integrity, stimulates
release of cytokines. Exotoxin A may
be important mediator of toxic shock
syndrome.
>135
0
<135
2
Creatinine (mcg/L)
Superantigens
Directly stimulates T-cell activation,
causing massive release of systemic
cytokines.
Hyaluronidase
Degrades hyaluronic acid.
<141
0
>141
2
Glucose (mmol/L)
<10
0
>10
1
Add partial scores for total LRINEC score; sum of >6 has a
high correlation with necrotizing infection, with a positive
predictive value of 92 percent and a negative predictive value
96 percent.
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UPMC
Table 3. Recommended Antibiotic Regimens for NSTI
Surgery
The most important determinant of survival in NSTI is prompt
surgical debridement. Several studies have shown that delay of
debridement beyond 24 hours after presentation is associated
Monotherapy
Agents
with increased mortality. 3-6 Radical excision of all devitalized
imipenem/cilastatin
meropenem
ertapenem
tissue should be performed until healthy, bleeding tissue is
piperacillin-tazobactam
encountered. Surgical findings consistent with NSTI include:
tigecycline
gray necrotic fascia, loss of resistance to blunt finger dissection
(i.e., the “finger test”), lack of bleeding tissue, and the presence
of foul-smelling “dishwater” fluid. Serial debridements spaced
Multidrug
Regimens
12 to 36 hours apart are generally the rule, because infections
penicillin or cephalosporin
PLUS aminoglycoside or fluoroquinolone
are rarely eradicated after the initial debridement. Initially, as with
PLUS clindamycin or metronidazole
all infected wounds, they should be left open and packed with
add vancomycin, linezolid, or daptomycin
for MRSA coverage if indicated
wet-dry dressings. Once infection is controlled, the patient may
benefit from negative-pressure wound therapy to assist with
add protein synthesis inhibitor in
severe or rapidly progressive infections
(clindamycin, linezolid)
granulation and wound closure15, though larger wounds may
ultimately require skin grafting.
Antibiotics
Impaired delivery of antibiotics to necrotic infected tissue can
limit their effectiveness locally, but antibiotics remain critical in
restricting bacterial spread and ameliorating systemic sepsis.
Empiric broad-spectrum antibiotic therapy directed against
Gram-positive cocci, Gram-negative rods, and anaerobes should
be instituted immediately. There is no single regimen that has
been advocated in the literature to date, and many single and
7,12
multidrug regimens have shown to be efficacious.
Hyperbaric Oxygen Therapy
Hyperbaric oxygen (HBO) therapy has been proposed as an
adjunct to surgery and antibiotics in the treatment of NSTI. The
technique involves the administration of 100 percent oxygen at a
pressure greater than 1 atmosphere absolute (ATA), resulting in a
dramatic increase in oxygen tension.16 Typical HBO therapy
involves administration at 2 to 3 ATA for 90 minutes three times
in the first 24 hours, then twice daily thereafter, though no
standard regimen has been established.
Special consideration should be given to antimicrobial coverage
of GAS and MRSA. Many would advocate the addition of
clindamycin to any empiric regimen, especially for coverage of
GAS.11 Because MRSA appears to be evolving as a significant
pathogen in NSTI, empiric therapy should include vancomycin,
daptomycin, or linezolid.12
Regardless of the initial regimen, antibiotic therapy should be
appropriately tailored to final microbiological speciation and
antibiotic sensitivity. Current guidelines recommend continuing
treatment until no further surgical debridement is necessary and
the patient’s physiology has normalized — typically a 10- to
14-day course.12
The proposed benefits of HBO include suppression of clostridial
њ-toxin production and generalized bacterial growth, enhancement
of leukocyte-killing activity and antibiotic effects, promotion of
tissue repair and wound closure, and bacteriocidal effects on
anaerobic organisms.16
Despite the physiologic rationale behind its use, clinical human
studies are limited mostly to case series and retrospective
analyses, and the data from these are inconsistent17-20. However,
many authors argue that the purported theoretical benefits and
relatively few major risks may support its use as an adjunct to
standard therapy.
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TR AUMA RO U NDS
Intravenous Immunoglobulin
Intravenous immunoglobulin (IVIG) is another adjunctive
measure that has been studied in patients with NSTI, primarily in
those with GAS or staphylococcal infections. Patients with NTSI
are deficient in antibodies recognizing streptococcal cell wallattachment proteins, which theoretically would be replaced with
pooled IVIG.10 Some small studies suggest a mortality benefit for
patients with NTSI treated with IVIG. While it is difficult to form
solid conclusions, some experts support the use of IVIG as an
6. Elliott DC et al. (1996) “Necrotizing soft tissue infections. Risk
factors for mortality and strategies for management.” Ann
Surg 224:672-683.
7. Elliott D et al. (2000) “The microbiology of necrotizing soft
tissue infections.” Am J Surg 179:361-366.
8. Sarani B et al. (2009) “Necrotizing fasciitis: current concepts
and review of the literature.” J Am Coll Surg 208(2):279-288.
9. Cainzos M et al. (2007) “Necrotizing soft tissue infections.”
Curr Opin Crit Care 13:433-439.
adjunct to surgery and antibiotics in critically ill patients with
NSTI secondary to streptococcal or staphylococcal species.
Conclusion
Though relatively uncommon, NSTIs are rapidly progressive
soft tissue infections that threaten both life and limb of affected
patients. Clearly, the major determinant of outcomes is the
rapidity with which the disease is diagnosed and surgical
debridement performed. Early, aggressive surgical debridement,
broad-spectrum antibiotics, and resuscitation form the cornerstone
of management. Most of these patients should be triaged to a
tertiary care facility that can provide the surgical and critical care
resources necessary to manage them. Adjunctive therapies such
as HBO, IVIG, and others may have real promise and the potential
to improve outcomes.
Gina M. Howell, MD, is a surgical resident, and Matthew R.
Rosengart, MD, MPH, is an associate professor of surgery
and critical care medicine at the University of Pittsburgh
School of Medicine.
References
1. Ellis Simonsen SM et al. (2006) “Cellulitis incidence in a
defined population.” Epidemio Infect 134:293-299.
2. Anaya DA et al. (2005) “Predictors of mortality and limb loss
in necrotizing soft tissue infections.” Arch Surg 140:151-158.
3. Mok MY et al. (2006) “Necrotizing fasciitis in rheumatic
disease.” Lupus 15:380-383.
4. Wong CH et al. (2003) “Necrotizing fasciitis: clinical
presentation, microbiology, and determinants of mortality.” J
Bone Joint Surg Am 85:1454-1460.
10. Johansson L et al. (2010) “Getting under the skin: the
immunopathogenesis of Streptococcus pyogenes deep tissue
infection.” Clin Infect Dis 51:58-65.
11. Mulla ZD. (2004) “Treatment options in the management of
necrotizing fasciitis caused by Group A Streptococcus.” Expert
Opin Pharmocother 5(8):1695-1700.
12. May AK et al. (2009) “Treatment of complicated skin and
soft tissue infections.” Surgical Infections 10(5):467-499.
13. Anaya DA et al. (2007) “Necrotizing soft tissue infection:
Diagnosis and management.” Clin Infect Dis 44:705-710.
14. Struk DW et al. (2001) “Imaging of soft tissue infections.”
Radiol Clin North Am 39:277-303.
15. Huang WS et al. (2006) “Use of vacuum-assisted wound
closure to manage limb wounds in patients suffering from
acute necrotizing fasciitis.” Asian J Surg 29:135-139.
16. Kaide CG et al. (2008) “Hyperbaric oxygen: Applications in
infectious disease.” Emerg Med Clin N Am 26:571-595.
17. Jallali N et al. (2005) “Hyperbaric oxygen as adjuvant therapy
in the management of necrotizing fasciitis.” Am J Surg
189:462-466.
18. Wilkinson D et al. (2004) “Hyperbaric oxygen treatment and
survival from necrotizing soft tissue infection.” Arch Surg
139:1339-1345.
19. Escobar SH et al. (2005) “Adjuvant hyperbaric oxygen
therapy for treatment of necrotizing fasciitis reduces mortality
…” Undersea Hyperb Med 32:437-443.
20. George ME et al. (2009) “Hyperbaric oxygen does not
improve outcomes in patients with necrotizing soft tissue
infection.” Surg Infect 10(1):21-28.
5. Voros D et al. (1993) “Role of early and extensive surgery in
the treatment of severe necrotizing soft tissue infection.” Br J
Surg 80:1190-1191.
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CALENDAR OF EVENTS
Continuing Education Classes
Name
Date
Time
Location
Cost
Cadaver Lab
May 31
6 to 8 p.m.
Ross West View EMS
5325 Perry Highway
Pittsburgh, PA 15229
None
AMLS Provider Course
Two days
May 31 & June 1
8 a.m. to 4 p.m.
(Both days)
Murrysville Medic One
3237 Sardis Road
Murrysville, PA 15668
UPMC/CMC Command
providers
$15.00
all other providers:
$50.00
ACLS/PALS Renewal
June 6
8 a.m. to 4 p.m.
Uniontown Firemen’s Ambulance
84 N. Beeson Blvd.
Uniontown, PA 15401
UPMC/CMC Command
providers
$5.00 per discipline
all other providers:
$45.00 per discipline
Advanced Burn Life
Support
June 27
8 a.m. to 4 p.m.
UPMC Mercy
Sr. M. Ferdinand Clark Auditorium
1400 Locust St.
Pittsburgh, PA 15219
$25
Fire Fighter Rehab
July 18
6 to 9 p.m.
Uniontown Firemen’s Ambulance
84 N. Beeson Blvd.
Uniontown, PA 15401
None
Advanced Burn Life
Support
Sept. 14
8 a.m. to 4 p.m.
UPMC Mercy
Sr. M. Ferdinand Clark Auditorium
1400 Locust St.
Pittsburgh, PA 15219
$25
Advanced Trauma Life Support 2011
June 18-19
July 19-20
Nov. 12-13
Dec. 3-4
June 19 (re-verification)
July 19 (re-verification)
Nov. 13 (re-verification)
Dec. 4 (re-verification)
For more information about ATLS courses, email [email protected] or call 412-647-8115.
For a list of nationally available ATLS courses, see http://web2.facs.org/atls/ATLSSearch.cfm?Search=USA.
Consider the opportunity to earn continuing education credits by reading Trauma Rounds and completing the corresponding continuing
education test. After reading, log on to http://www.upmc.com/Services/EmergencyMedicine/prehospital-care/Pages/TraumaRounds.aspx.
On the Trauma Rounds website, you can print the test and mail the completed version back to UPMC, or you can take the test online
through the Pennsylvania Department of Health’s online testing program.
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