The Journal of Emergency Medicine, Vol. 42, No. 2, pp. 127–132, 2012
Copyright © 2012 Elsevier Inc.
Printed in the USA. All rights reserved
0736-4679/$–see front matter
doi:10.1016/j.jemermed.2010.05.007
Original
Contributions
ABNORMAL COAGULATION TESTS OBTAINED IN THE EMERGENCY
DEPARTMENT ARE ASSOCIATED WITH MORTALITY IN PATIENTS WITH
SUSPECTED INFECTION
Christopher M. Fischer,
MD,*
Kiichiro Yano,
PHD,†
William C. Aird,
MD,†
and Nathan I. Shapiro,
MD, MPH*†
*Department of Emergency Medicine and †The Center for Vascular Biology Research and Division of Molecular and Vascular
Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts
Reprint Address: Christopher M. Fischer, MD, Department of Emergency Medicine, Beth Israel Deaconess Medical Center, 1
Deaconess Road, CC2-W, Boston, MA 02215
e Abstract—Background: Early recognition of acute organ dysfunction in emergency department (ED) patients
with suspected infection may help select patients at increased risk of mortality. The hematologic system is often
overlooked in the evaluation and management of patients
with infection because it is poorly circumscribed and serves
a multitude of functions. Study Objectives: We examine the
hypothesis that abnormalities in commonly and easily obtained markers of coagulation function (international normalized ratio [INR], partial thromboplastin time [PTT],
and platelet count [PLT]) are associated with mortality in
ED patients admitted to the hospital with suspected infection. Methods: Design: Secondary analysis of a prospective
observational cohort study. Setting: Urban tertiary care
university hospital with 50,000 annual ED visits. Patients:
Included patients: adults (age 18 > years) evaluated in the
ED for a suspected infection, had an INR, PTT, and PLT
obtained during the ED stay, admitted to the hospital.
Excluded patients: on oral anticoagulant therapy, received
heparin, or pre-existing severe liver disease. Results: There
were 1688 patients included. The in-hospital mortality rate
was 5.9%. After adjusting for elderly status, comorbid
illness burden, and severity of illness, elevated INR was
associated with a 2.9 (95% confidence interval [CI] 1.6 –
5.2) increased odds of death, and a low platelet count
(< 150,000/uL) was associated with 2.0 (95% CI 1.2–3.3)
increased odds of death. The C-statistic for the model was
0.80. Conclusion: We found an independent association
between abnormalities in the coagulation system and mor-
RECEIVED: 22 August 2009; FINAL
ACCEPTED: 2 May 2010
SUBMISSION RECEIVED:
tality in ED patients with suspected infection. These findings underscore the close interaction between inflammation
and coagulation and provide evidence that these simple
laboratory tests should be routinely considered during the
early evaluation of the infected patient. © 2012 Elsevier
Inc.
e Keywords— coagulation; hematology; infection
INTRODUCTION
There are an estimated 750,000 cases of severe sepsis
and septic shock annually in hospitalized patients in the
United States, with an estimated in-hospital mortality
rate of over 30% (1). Nearly two-thirds of these patients
are initially evaluated in the emergency department (ED)
(2). Early identification and treatment of severe sepsis in
the ED can improve morbidity and mortality (3,4). Early
recognition of acute organ dysfunction in ED patients
with suspected infection may help select patients at increased risk of mortality who may benefit most from
aggressive treatment strategies (5,6).
The hematologic system is often overlooked in the
evaluation and management of patients with sepsis syndromes. Unlike other organ systems, the hematologic
system is poorly circumscribed, and serves a multitude of
functions (7). Regulation of coagulation occurs through a
7 December 2009;
127
128
C. M. Fischer et al.
balance of anti- and procoagulant proteins, which are
synthesized in the liver, endothelium, and circulating
cells. Red blood cells, white blood cells, and platelets are
involved in both the local and systemic response to
invading pathogens, and are widely distributed throughout the body. Together, these different components play
an important role in oxygen delivery, hemostasis, and
defense against pathogens.
The interactions between the inflammatory and coagulation systems are becoming increasingly understood at
the cellular level (8). In vitro and in vivo studies in
animals and humans demonstrate that inflammatory responses shift the hemostatic balance to favor a procoagulant state. In extreme cases, this can manifest as
disseminated intravascular coagulation (9). Inflammatory
mediators have a multiplicity of effects on markers of
coagulation, including elevated platelet count, altered
platelet reactivity, increased platelet consumption, downregulation of natural anticoagulant mechanisms, and impaired fibrinolysis. Collectively, these changes lead to
initiation and propagation of coagulation (8).
To date, most of the studies examining the relationship between inflammation and coagulation have either
examined the development of disseminated intravascular
coagulation (DIC), or have assessed the role of biomarkers of coagulation activation that are not commonly
assessed in clinical practice (e.g., antithrombin, plasminogen activator inhibitor, protein C) (10 –14). To examine
the importance of changes in the hemostatic system in
ED patients with suspected infection, we undertook the
current study to examine the hypothesis that abnormalities in commonly and easily obtained markers of coagulation function (international normalized ratio [INR],
partial thromboplastin time [PTT], and platelet count
[PLT]) are associated with mortality in ED patients admitted to the hospital with a suspected infection.
MATERIALS AND METHODS
Study Design
This was a secondary analysis of a prospective observational cohort study. The study was approved by the
Institutional Review Board at our institution.
Study Setting and Population
Consecutive patients were enrolled at an urban tertiary care
university hospital with approximately 50,000 annual ED visits. The study enrollment period was between September 18,
2005 and September 30, 2006. We included all adult patients
(age 18 years or older) who were evaluated in the ED for a
suspected infection as determined by the treating physician,
had an INR, PTT, and PLT obtained during the ED stay, and
were subsequently admitted to the hospital. Patients were excluded if they were on oral anticoagulant therapy at the time of
ED evaluation, if they received intravenous heparin during
their ED stay, or if they had a pre-existing diagnosis of severe
liver disease, which was defined a priori as any patient who
had a previous diagnosis of decompensated or end-stage liver
disease by their primary care physician or hepatologist as
determined by medical record review at the time of admission.
Study Protocol
Patients were identified prospectively and their ED charts were
reviewed and abstracted without knowledge of the patient’s
hospital course using a previously described methodology that
has been shown to exhibit a high degree of inter-rater reliability
in identifying patients with suspected infection (15). In brief,
we reviewed the daily list of ED admissions to screen for
patients with an admission diagnosis consistent with infection
(e.g., pneumonia) or possibly consistent with infection (e.g.,
shortness of breath). Trained research assistants reviewed and
abstracted the ED medical records of eligible patients to confirm that the ED clinicians had a clinical suspicion of infection
at the time of admission. This was determined by reviewing
the medical decision-making portion of the emergency physician’s notes and by the decision to give antibiotics. Only
information that was available during the ED course (i.e.,
before admission) was abstracted. Outcome data were not
available during this phase of data collection. Pertinent demographic data and components of history, physical examination,
and vital sign information were recorded using a structured
data collection instrument. Laboratory values were collected,
and the suspected source of infection was derived from the
medical decision-making portion of the chart. To limit the
possibility of bias, outcome data were collected separately
using the hospital’s information systems.
Comorbidity status was assessed using the Charlson comorbidity index (16). The Charlson index has been shown to
be associated with 1-year mortality in ED patients with suspected infection (17). Severity of illness was determined using
the Mortality in Emergency Department Sepsis (MEDS) score
(15). The MEDS score has been shown to be associated with
both in-hospital and 1-year mortality in ED patients with suspected infection, and externally validated in a multi-center
study (15,18,19). To avoid collinearity in the regression model,
the platelet count and age components of the MEDS score
were excluded, resulting in a modified MEDS score
(mMEDS). The end-stage liver disease component of the
Charlson score was excluded, resulting in a modified Charlson
score. The mMEDS and modified Charlson scores were reported as continuous variables. The primary outcome of interest was in-hospital mortality rate.
Abnormal Coagulation Tests and Mortality in the ED
129
Table 1. Important Demographic, Clinical, and Laboratory Abnormalities for the Total Population, and Stratified by
Mortality Status
Demographics
Age (SD)
% Male
Modified Charlson comorbidity score (SD)
Modified MEDS score
Labs
INR (SD)
PTT, seconds (SD)
PLT, ⫻1000/uL (SD)
Suspected source of infection (%)*
Pneumonia
Urinary tract
Skin/soft tissue
Intra-abdominal (includes biliary and perforated viscus)
*Other
All Patients
(n ⫽ 1688)*
Survivors
(n ⫽ 1588)*
Non-survivors
(n ⫽ 100)*
63.8 (19.0)
48%
1.6 (1.9)
2.8 (2.7)
62.8 (18.7)
48%
1.6 (1.9)
2.60 (2.6)
70.4 (18.7)
60%
3.2 (2.9)
4.9 (3.0)
1.25 (0.5)
27.9 (11.7)
273 (138)
1.2 (0.5)
27.8 (11.2)
267 (138)
1.6 (0.9)
34.2 (22)
261 (178)
22%
14%
14%
10%
47%
21%
14%
14%
10%
47%
36%
14%
4%
6%
53%
The “other” category includes meningitis, endocarditis, line infection, as well as fever without a source or suspected infection without
a clearly identifiable source in the ED.
* Patients could have multiple sources of infection recorded.
SD ⫽ standard deviation; MEDS ⫽ Mortality in Emergency Department Sepsis; INR ⫽ international normalized ratio; PTT ⫽ partial
thromboplastin time; PLT ⫽ platelet count.
Statistical Methods
Laboratory test results were classified as normal or abnormal using clinically relevant thresholds determined a
priori: INR ⬎ 1.5, PTT ⬎ 35 s, PLT ⬍ 150,000/uL. The
INR and PLT thresholds were chosen due to their clinical
use and their use as thresholds in other studies (15). The
PTT threshold was chosen because it is the upper limit of
normal in our clinical laboratory. We built a multiple
logistic regression model to adjust for potential confounders, including elderly status (age ⬎ 65 years), severity of illness (modified MEDS score), and comorbid
burden (modified Charlson score) to assess whether coagulation parameters were, in fact, independent predictors of mortality in sepsis. The C-statistic was reported as
a measure of model performance. All statistics were
analyzed using JMP 7.0 (SAS Institute, Cary, NC).
RESULTS
There were a total of 1688 patients who met the inclusion
criteria. During the time of enrollment, there were 5638 patients evaluated in the ED with suspected infection, of which
4151 patients were admitted to the hospital. There were 1765
patients excluded because they did not have all three laboratory
tests obtained during their ED stay. Patients had a mean age of
63.8 (⫾SD 19) years, and 48% were male (Table 1). The most
commonly identified suspected sources of infection were lung
(21%), skin and soft tissue (14%), and urinary tract (13%). The
mean modified Charlson score was 1.6 (⫾ 1.9), and the mean
mMEDS score was 2.8 (⫾ 2.7). The in-hospital mortality rate
was 5.9%.
The mean INR was 1.25 (⫾ 0.5), and 8.1% (136/
1552) of all patients had an INR ⬎ 1.5. The mean PTT
was 27.9 s (⫾11.7), and 7.2% (121/1688) of all patients
had a PTT ⬎ 35 s. The mean platelet count was
272,000/uL (⫾ 138,000/uL), and 14.7% (249/1688) of
all patients had a platelet count ⬍ 150,000/uL.
After adjusting for elderly status (age ⬎ 65 years),
comorbid illness burden (Charlson score), and severity of
illness (mMEDS score), elevated INR (⬎ 1.5) was associated with a 2.9 (95% confidence interval [CI] 1.6 –5.2)
increased odds of death, and a low platelet count (⬍
150,000/uL) was associated with 2.0 (95% CI 1.2–3.3)
increased odds of death (Table 2). The PTT was not
independently associated with increased mortality in this
model. The C-statistic for the model was 0.80.
Table 2. Odds of Mortality for Covariates Included in
Logistic Regression
Variable
Odds Ratio
95% CI
Intercept
INR ⬎ 1.5
Platelets ⬍ 150,000/uL
Age ⬎ 65 years
mMEDS
mCharlson
2.9
2.0
2.0
1.2
1.3
1.6–5.2
1.2–3.3
1.2–3.2
1.1–1.3
1.2–1.4
The C-statistic representing the area under the curve for model
accuracy was 0.80.
CI ⫽ confidence interval; INR ⫽ international normalized ratio.
130
C. M. Fischer et al.
DISCUSSION
We found that abnormalities coagulation markers occurred
in 7–15% of patients in our cohort, and that abnormalities in
INR and platelet count were significantly associated with
mortality in ED patients with suspected infection. These
findings underscore the close interaction between inflammation and coagulation and the importance of the coagulation cascade in sepsis. Furthermore, this study provides
evidence that these simple laboratory tests should be routinely considered during the early evaluation of the infected
patient. Prior studies, most notably the Activated Protein C
Worldwide Evaluation in Severe Sepsis (PROWESS) trial,
have demonstrated that in patients with severe sepsis and
septic shock, activation of coagulation and inflammatory
pathways are virtually universal phenomena (13,20). In
patients who do not fulfill the criteria for overt DIC, many
have been shown to have an evolving coagulopathy, as
demonstrated by worsening coagulation tests (10). The current criteria for non-overt DIC assess the pattern of change
in coagulation tests such as the PLT, prothrombin time
(PT), and D-dimer, along with additional specialized tests
such as protein C and antithrombin levels. Our study is
different from these prior studies because it includes all ED
patients with suspected infection, and includes only coagulation tests commonly and easily obtained in the ED.
Systemic inflammation, as a result of infection, is
associated with activation of primary and secondary hemostasis. Activation of primary hemostasis is manifested
by thrombocytopenia in 35–59% of patients (7). Activation of secondary hemostasis is manifested by increased
circulating levels of D-dimers in virtually all patients
with severe sepsis, decreased protein C levels in up to
90% of such patients, and reduced antithrombin III
(ATIII) levels in more than half of patients (11,13,14,21).
Marked activation of coagulation and secondary consumption of clotting factors may lead to the clinical
syndrome of DIC, characterized by widespread fibrin
deposition and thrombosis of small and midsize vessels,
along with uncontrolled bleeding resulting from consumption of platelets and coagulation proteins. However,
in contrast to the universal finding of coagulation activation in patients with severe sepsis, DIC is estimated to
occur in only 15–30% of these individuals (22,23).
Several mechanisms have been implicated in the development of thrombocytopenia in sepsis, including de
novo ethylenediaminetetraacetic acid-dependent antibodies and secondary pseudothrombocytopenia, immune
mechanisms, hematophagocytosis, platelet sequestration
on activated endothelium, and consumption in DIC
(7,24 –27). Activation of the blood clotting mechanism in
sepsis is initiated by tissue factor expression on the
surface of circulating monocytes, tissue macrophages,
and, possibly, subsets of endothelial cells (28). Sepsis is
also associated with an attenuation of anticoagulant
mechanisms, including protein C and ATIII levels, and
the fibrinolytic pathway (29,30). Moreover, sepsis-mediated
downregulation of thrombomodulin and endothelial protein C receptor on the endothelial cell surface may impair
activation of protein C (31).
The above changes may have prognostic implications.
For example, thrombocytopenia is associated with higher
mortality in patients with severe sepsis (32). The degree
and duration of thrombocytopenia, as well as the net
change in the platelet count, are important determinants
of survival (33). Low levels of circulating ATIII and
protein C are predictive of poor survival (14,34). In
clinical studies of multiple organ dysfunction, maximum
PT and PTT were shown to be longer in non-survivors
than in survivors (35). Other studies have reported that
DIC is an independent predictor for mortality in patients
with sepsis (36). However, DIC is often a late complication of overwhelming infection, rather than a presenting symptom. This study represents an attempt to understand the importance of coagulation dysfunction early in
the examination of patients with suspected infection.
Limitations
This study has a number of limitations. We used the
inclusion criteria of all ED patients who were admitted to
the hospital and had INR, PTT, and PLT obtained in the
ED. There are certainly patients with potential infection
who did not have all three laboratory tests obtained in the
ED, which could have led to a selection bias. Although
platelet counts are nearly universally obtained on all
patients admitted with a suspected infection, it is possible
that clinicians obtained INR and PTT on patients who
were suspected to be more ill, and therefore more likely
to die during their hospitalization. Coagulation abnormalities may be confounded by other covariates that
were not measured, and the increased risk of mortality
that we found may not represent the true association
between these parameters and mortality. Additionally,
we used the outcome of death by any cause due to its
robust nature, but patients may have had deaths not
attributable to infection. The covariates that we used
were obtained from the ED chart, which may be incomplete or inaccurate, leading to a misclassification bias.
This was a single-center study, and prospective validation on a different patient population is required to assess
the generalizability of our findings.
CONCLUSION
We found a statistically significant, independent association between abnormalities in the coagulation system
Abnormal Coagulation Tests and Mortality in the ED
(INR and PLT) and mortality in ED patients with suspected infection. These findings are potentially useful
when identifying which patients require admission to the
hospital, higher levels of care (e.g., step-down or intensive care unit), and when selecting patients for more
aggressive sepsis therapies.
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ARTICLE SUMMARY
1. Why is this topic important?
Recognition of acute organ dysfunction in emergency
department (ED) patients with suspected infection may
help select patients at increased risk of mortality.
2. What does this study attempt to show?
This study examines the hypothesis that abnormalities
in commonly and easily obtained markers of coagulation
function (international normalized ratio [INR], partial
thromboplastin time, and platelet count) are associated
with mortality in ED patients admitted to the hospital
with suspected infection.
3. What are the key findings?
After adjusting for elderly status, comorbid illness
burden, and severity of illness, elevated INR or low
platelet count was associated with a increased odds of
death.
4. How is patient care impacted?
These findings underscore the close interaction between inflammation and coagulation, and provide evidence that these simple laboratory tests should be routinely considered during the early evaluation of the
infected patient.