American Journal of Emergency Medicine 35 (2017) 1755–1758

Contents lists available at ScienceDirect

American Journal of Emergency Medicine

journal homepage: www.elsevier.com/locate/ajem

Review

Evaluation of fever in the emergency department☆,☆☆

Sarah DeWitt, MD a, Summer A. Chavez, DO, MPH a, Jack Perkins, MD a, Brit Long, MD b,⁎, Alex Koyfman, MD c
a
Virginia Tech-Carilion School of Medicine and Research Institute, Department of Emergency Medicine, 1 Riverside Circle, Roanoke, VA 24014, United States
b
San Antonio Military Medical Center, Department of Emergency Medicine, 3841 Roger Brooke Dr, Fort Sam Houston, 78234, TX, United States
c
The University of Texas Southwestern Medical Center, Department of Emergency Medicine, 5323 Harry Hines Boulevard, Dallas, 75390, TX, United States

a r t i c l e i n f o a b s t r a c t

Article history: Background: Fever is one of the most common complaints in the emergency department (ED) and is more com-
Received 22 June 2017 plex than generally appreciated. The broad differential diagnosis of fever includes numerous infectious and non-
Received in revised form 12 August 2017 infectious etiologies. An essential skill in emergency medicine is recognizing the pitfalls in fever evaluation.
Accepted 13 August 2017 Objective of review: This review provides an overview of the complaint of fever in the ED to assist the emergency
physician with a structured approach to evaluation.
Keywords:
Discussion: Fever can be due to infectious or non-infectious etiology and results from the body's natural response
Fever
Blood cultures
to a pyrogen. Adjunctive testing including C-reactive protein, erythrocyte sedimentation rate, and procalcitonin
Core temperature has been evaluated in the literature, but these tests do not have the needed sensitivity and specificity to defini-
Inflammatory markers tively rule in a bacterial cause of fever. Blood cultures should be obtained in septic shock or if the results will
Pulmonary embolism change clinical management. Fever may not be always present in true infection, especially in elderly and immu-
nocompromised patients. Oral temperatures suffer from poor sensitivity to diagnose fever, and core tempera-
tures should be utilized if concern for fever is present. Consideration of non-infectious causes of elevated
temperature is needed based on the clinical situation.
Conclusion: Any fever evaluation must rigorously maintain a broad differential to avoid pitfalls that can have pa-
tient care consequences. Fever is complex and due to a variety of etiologies. An understanding of the pathophys-
iology, causes, and assessment is important for emergency physicians.
Published by Elsevier Inc.

1. Introduction
Fever is one of the most common patient complaints in the Emer-
gency Department (ED), accounting for approximately 15% of visits in
the elderly and 5% in adults [1]. While many fevers represent an infec-
tious source of pathology, other sources of fever include pulmonary em-
bolism, intracranial hemorrhage, medication, or malignancy (see Table
1). There are numerous potential pitfalls both in failing to consider
non-infectious etiologies of fever but also in the infectious evaluation
of fever. This review focuses on infectious sources of fever, the pitfalls
☆ Conflicts of interest: None.
☆☆ Acknowledgements: This manuscript did not utilize any grants, and it has not been
presented in abstract form. This clinical review has not been published, it is not under con-
sideration for publication elsewhere, its publication is approved by all authors and tacitly
or explicitly by the responsible authorities where the work was carried out, and that, if ac-
cepted, it will not be published elsewhere in the same form, in English or in any other lan-
guage, including electronically without the written consent of the copyright-holder. This
review does not reflect the views or opinions of the U.S. government, Department of
Defense, U.S. Army, U.S. Air Force, or SAUSHEC EM Residency Program.
⁎ Corresponding author at: 3841 Roger Brooke Dr, Fort Sam Houston, TX 78234, United
States.
E-mail addresses: sadewitt@carilionclinic.org (S. DeWitt), brit.long@yahoo.com
(B. Long).
in testing, situations when fever may not be present yet the patient
does indeed have infectious pathology, and finally some considerations
involving non-infectious causes of fever.
2. Discussion
2.1. Fever pathophysiology
Fever, also known as pyrexia, results from an increase in the body's
temperature set point. The hypothalamus controls body temperature
by balancing inputs from the peripheral nerves that utilize warm/cold
receptors in the skin, while also analyzing the temperature of blood in
the surrounding area [3,4]. Fever is typically caused by a pyrogen, a
chemical substance that provokes fever. One such example is an exoge-
nous pyrogen, such as those seen in gram-positive bacteria (Staphylo-
coccus aureus enterotoxins) and the superantigens associated with
Group A streptococcus and Group B streptococcus microbial infections
[1,3]. Many bacteria and fungi trigger the production and release of cy-
tokines, small proteins that trigger the inflammatory cascade. These cy-
tokines lead to prostaglandin-2 release in peripheral tissues, raising the
hypothalamic temperature set point through cAMP release [1,3]. This
process also occurs in malignancy, autoimmune diseases, and other

http://dx.doi.org/10.1016/j.ajem.2017.08.030
0735-6757/Published by Elsevier Inc.
1756 S. DeWitt et al. / American Journal of Emergency Medicine 35 (2017) 1755–1758

disease states that cause inflammation. Central nervous system cyto- in selected cases. Blood cultures may not be necessary in cases of urinary
kines are responsible for the hyperpyrexia seen in neurologic trauma tract infection (UTI) or pneumonia in patients being discharged; how-
and infection [1,3]. A 2015 randomized controlled study from the New ever, they would be useful in cases of severe sepsis or septic shock to
England Journal of Medicine evaluated treatment of fever with acetamin- further tailor antibiotic therapy. Adjunctive serologic testing such as C-
ophen in the intensive care unit, finding fewer ICU-free days in those reactive protein (CRP), erythrocyte sedimentation rate (ESR), and
given acetaminophen versus placebo [5]. However, the study failed to procalcitonin may be utilized to further refine the clinical suspicion of
show a mortality benefit in treating fever at 28 days or 90 days [5]. infectious pathology [6,7].
C-reactive protein is an acute phase reactant that rises in response to
2.2. Infectious vs. non-infectious inflammatory stimuli. Serum CRP levels surge within 4–6 h after stimu-
lation, double every 8 h, and peak after 35–60 h [8,9]. In patients who
When evaluating a febrile patient in the ED, a key clinical question is present with fever onset N 12 h, serum CRP is elevated significantly in
whether infection is likely enough to warrant antimicrobial administra- those with bacterial infections [10]. The initial form of CRP testing was
tion. A detailed history and physical examination, the past medical his- qualitative and positive in almost all disease states. Since then, a specific
tory, current medications (e.g. chemotherapy, glucocorticoids), and monoclonal antibody and immunological methods of measurement are
recent use of antibiotics help shape the pre-test probability of infection. available, making the current CRP test more valuable in clinical practice.
However, it is common to utilize laboratory testing and radiographic In a review published by Povoa in 2002, a CRP value between 50 and
imaging to further evaluate the source of fever. Basic testing in the ED 79 mg/l had sensitivity for sepsis between 72 and 98% and specificity be-
often involves a complete blood count (CBC), urinalysis (UA), and tween 66 and 75% [7].
Chest X-ray (CXR). The emergency physician (EP) may deem it appro- Unfortunately, C-reactive protein is non-specific and has been found
priate to send urine culture, blood cultures, and add viral antigen testing to be elevated in numerous other conditions such as malignancy, ob-
structive sleep apnea, and chronic vascular disease [11-13]. It is used
Table 1 most frequently to provide adjunctive information in the search for
Differential diagnosis of fever in the emergency department [1,2]. more unusual sources of infection, such as osteomyelitis. It should not
Infectious causes of fever Non-infectious causes of fever be used as a stand-alone test to confirm or exclude infection as the
Bacterial infections Malignancy (e.g. leukemia, lymphoma,
cause of fever.
pheochromocytoma) Much like CRP, erythrocyte sedimentation rate (ESR) is occasionally
Autoimmune (e.g. rheumatoid arthritis, systemic utilized in the ED often as an adjunctive piece of information. However,
– UTI
lupus erythematosus) it suffers from a lack of specificity especially in the older population with
– Tubo-ovarian abscess
Drug reaction
– Prostatitis numerous comorbid conditions [14]. It should not be relied upon alone
– Meningitis to exclude or confirm an infectious source of fever.
– Cavernous sinus – Allergic reaction Procalcitonin (PCT) is a 116-amino acid peptide that rises in re-
thrombosis – Metabolic consequences of drug
sponse to infectious etiologies. It is much more likely to be elevated in
– Brain abscess – Ingestion (anticholinergic, sympathomimetic)
– Cholangitis Seizure bacterial, as opposed to viral infections [15,16]. Serum procalcitonin
– Appendicitis Environmental fever levels increase significantly in severe systemic infections [15]. The use
– Cholecystitis of PCT in the clinical setting to diagnose and treat acute respiratory in-
– Diverticulitis fections has been shown to decrease overall antibiotic consumption,
– High external temperatures (e.g. heat stroke)
– Cellulitis
– Necrotizing fasciitis
– Excess exercise however there is no mortality benefit from the use of PCT [17]. Currently
Hyperthyroid its use is not prevalent in the ED, and it has not been validated in the ED
– Osteomyelitis
– Pneumonia to support decisions regarding antibiotic use in patients with severe
– Retropharyngeal ab- – Thyroid storm sepsis or septic shock. Much like CRP and ESR, it is an adjunctive piece
scess Neurologic of information EPs may use to help shape their pre-test probability of
– Otitis media
– Sinusitis infection.
– Endocarditis – Intracranial/subarachnoid hemorrhage
– Pericarditis Embolic vs. Thrombosis vs. Infarction 2.3. Blood cultures in fever
– Myocarditis
Viral infections
– Myocardial infarction The potential utility and indication for blood cultures in the febrile
– Renal infarct patient is a frequent concern in the ED. Blood cultures are generally
– Pharyngitis – Pulmonary embolus
Blood transfusion reaction
not recommended in patients who will be discharged, have uncompli-
– Gastroenteritis
– Aseptic meningitis Factious fever cated infectious disease presentations, or in situations where the results
– HIV of the cultures will not change management [18]. However, in patients
– Influenza with severe sepsis or septic shock, it is incumbent upon EPs to try and
– Munchausen's vs. Munchausen's by proxy
Parasitic infections obtain blood cultures prior to initiation of antibiotics [18]. Patients
Neuroleptic malignant syndrome
Malignant hyperthermia who are immunocompromised (e.g. diabetes, cirrhosis) have a higher
– Malaria Serotonin syndrome likelihood of bacteremia with infectious pathology and may warrant
– Toxoplasmosis blood cultures even if they are stable and will be admitted to a non-
– Giardiasis
Arthropod infections
ICU setting [18]. Additionally, it is important to be aware of situations
where blood cultures may be needed to detect clinically important in-
fectious diseases such as occult bacteremia due to S. aureus, as this
– Lyme
– Rocky Mountain
often leads to worse clinical outcomes and cannot be diagnosed without
Spotted fever blood cultures [19]. Blood cultures should also be obtained in cases of
– Babesiosis septic shock [18,20]. In cases of unclear benefit, it is reasonable to dis-
Fungal infections cuss with the admitting provider whether blood cultures are warranted.
Such situations could include hemodynamically stable (i.e. will not re-
– Candidiasis quire ICU level of care) patients being admitted for community-ac-
– Blastomycosis quired pneumonia or cellulitis [20]. This course of action promotes
– Histoplasmosis
antimicrobial stewardship, as there is a risk of false positive blood
 S. DeWitt et al. / American Journal of Emergency Medicine 35 (2017) 1755–1758
cultures resulting in unnecessary and often broad-spectrum antibiotics.
For example, in patients with community-acquired pneumonia, the es-
timated false-positive blood culture rate approaches 8% [21].
2.4. Obtaining temperatures: oral vs. core temperatures
Oral temperatures are more convenient than core temperatures and
are often obtained with the initial set of vital signs. However, evidence
does not support the accuracy of oral temperatures. A 2015 meta-anal-
ysis revealed that peripheral temperatures are unacceptable for making
clinical decisions [22]. Seventy-five studies were included that com-
pared a gold standard core temperature to peripheral temperatures.
The authors used ±0.5 °C as the accepted limit of agreement. In patients
with hyperthermia, the limits of agreement were − 1.44 °C to 1.46 °C
and in hypothermia, − 2.07 °C to 1.90 °C. The calculated sensitivity
was only 64% (95% confidence interval [CI]: 55–72%) but specificity per-
formed better at 96% (95% CI: 93–97%) [23].
Thus, if the patient is febrile or hypothermic by oral temperature, it
does not need to be repeated. However, if the patient is normothermic
by an oral temperature and the result would change provider manage-
ment (e.g. sepsis is high on the differential), a core temperature is
strongly recommended either by a rectal thermometer or tempera-
ture-sensing Foley catheter.
2.5. Fever and sepsis
The Systemic Inflammatory Response Syndrome (SIRS) criteria em-
brace hyperthermia and hypothermia as parameters to define sepsis.
These criteria have come under scrutiny in recent years, and there is
no better example as to the pitfalls of the SIRS criteria than the afebrile
septic patient. In the elderly and the immunocompromised patient (e.g.
HIV/AIDS, cancer, cirrhosis, diabetes mellitus, systemic corticosteroid
use, organ transplant, use of immunosuppressant medications), the fe-
brile response to infection can be absent. Wester et al. report 20–30%
of elderly patients may either remain afebrile or mount a blunted re-
sponse to infection [24]. Other studies have shown that in elderly pa-
tients with bacteremia, a lack of fever is independently associated
with 30-day mortality [25]. A study by Fernandes et al. highlighted
this risk in elderly patients with bacterial meningitis [26]. They found
factors that were independently associated with adverse clinical out-
comes included older age, absence of fever at ICU admission, and
lower Glasgow Coma Scale/Score [26].
Caterino et al. reported that only absence of fever on initial presenta-
tion to the ED and initial serum bicarbonate level independently pre-
dicted patient decompensation after admission to a floor bed as
defined by a transfer to the ICU within 48 h of admission [27]. One po-
tential conclusion from this study is that the diagnosis of sepsis, subse-
quent treatment, and assessment of severity of illness are made more
complex in the afebrile patient. The literature has demonstrated many
cases of atypical presentation (i.e. afebrile, non-specific complaints
such as weakness) in elderly patients who are bacteremic [28].
In sum, patients with sepsis may not demonstrate fever. The older
patient and those who are immunocompromised should be expected
to present in atypical fashion, and sepsis should be considered regard-
less of a documented fever. A 2017 article in Critical Care Medicine high-
lights this concept succinctly, as it reports a lower mortality in patients
who had a fever associated with severe sepsis and septic shock. The au-
thors even note they determined the febrile patient cohort received
“better quality of care” most likely due to earlier suspicion of sepsis as
a result of the fever [29].
In contrast to the SIRS criteria, the qSOFA (quick Sepsis Related
Organ Failure Assessment) score does not account for hypothermia or
hyperthermia. While the qSOFA is advocated for use in the ED by the So-
ciety for Critical Care Medicine, it should be noted that this score was
designed to predict mortality and not to identify sepsis [30].
1757
2.6. Fever from non-infectious sources
Not all fever is from an infectious etiology. Pulmonary embolism
(PE), intracranial hemorrhage (ICH), neuroleptic malignant syndrome
(NMS), serotonin syndrome, toxic ingestion (salicylate, sympathomi-
metic drug toxicity, etc.), thyroid storm, and heat stroke are among
the numerous life-threatening causes of non-infectious fever.
Body temperature ≥ 106.7 °F defines hyperpyrexia [3]. While this
may occur in sepsis, this is more common in those with ICH, NMS, and
heat stroke (see Table 2) [3,23]. Additionally, there is marked difference
between hyperthermia and fever. Hyperthermia does not respond to
typical anti-pyretics since there are no pyrogenic molecules [3]. It is im-
portant to consider the history immediately before presentation, such as
prolonged exposure in a hot environment consistent with heat stroke or
ingestions. Prior history of thyroid disease should be assessed. Rare pa-
tients will have fever due to pathology directly affecting their hypothal-
amus such as tumor, trauma, or hemorrhage, termed “hypothalamic
fever.” [3].
In patients with undifferentiated hyperpyrexia, the differential in
Table 2 can guide the evaluation. Most of these etiologies have specific
treatments and high associated mortality if not treated. A thorough re-
view of the history and current medications is critical to an accurate
diagnosis.
Fever, especially low-grade fever, is commonly seen with pulmonary
embolism (PE) [31-33]. However, any clinical significance remains to be
determined. Two historical studies from the 1970s reported fever in 50%
(N 37.5 °C) and 57.1% (N38 °C) of patients with pulmonary embolism,
respectively [31-33]. However, the landmark Prospective Investigation
of Pulmonary Embolism Diagnosis (PIOPED) study reported a much
lower rate of fever in patients with PE [34]. Investigators found that
14% of patients with fever (≥ 100.0 °F) had no identifiable source of
that fever other than PE [34]. The incidence of pulmonary hemorrhage
or infarction was not statistically significant in those with fever. Calvo-
Romero et al. performed a retrospective review of 154 patients with
acute PE and found 18.2% had fever (N 37 °C) without any other
known causes [34].
Conversely, a high-grade fever (≥101 °F) was present in only 6% of
the study group in the PIOPED trial [34]. In the Calvo-Romero study,
27 of 28 patients had a low-grade fever (temperature between 37 °C
and 39 °C) [35]. In this study, electrocardiogram findings, mortality
rates, and CXR findings were similar in patients with PE regardless of
the presence of fever. In the PIOPED study, 37% of patients who died
with a pulmonary embolism had a low-grade fever [34]. Higher-grade
fevers were more likely to be associated with secondary pneumonitis
or widespread pulmonary infarction in the PIOPED group. Unfortunate-
ly, it is not uncommon for the EP to encounter the dilemma of whether a
febrile patient with respiratory complaints has a pulmonary embolus or
is septic from pneumonia. The clinician must vigorously review the his-
tory, examination, and any ancillary testing (e.g. CXR) to narrow the dif-
ferential diagnosis. Advanced imaging such as computed tomography of
the pulmonary vasculature may be required to differentiate sepsis from
pulmonary embolus if the CXR is non-diagnostic.
Table 2
Hyperpyrexia [2,3].
Hyperpyrexia differential in the ED
Sepsis
Heat exposure/heat stroke
Neuroleptic malignant syndrome
Malignant hyperthermia
Serotonin syndrome
Intracranial hemorrhage
Thyroid storm
Anticholinergic toxidrome (e.g. tricyclic antidepressants)
Sympathomimetic toxidrome (e.g. amphetamines, cocaine)
1758 S. DeWitt et al. / American Journal of Emergency Medicine 35 (2017) 1755–1758
3. Conclusions
A chief complaint of fever or discovering fever in the ED often drives
the differential diagnosis in the direction of infectious etiologies. While
the EP may decide that an evaluation of a potential infectious etiology is
warranted, it is important to consider that fever only represents the
body's response to a pyrogen, and numerous non-infectious etiologies
can produce or function as a pyrogen. Adjunctive testing such as CRP,
ESR, and procalcitonin may be of value in determining the probability
of an infectious source but are hindered by a lack of specificity. Blood
cultures are not a routine part of the evaluation of fever and should be
utilized in clinical scenarios which are evidence-based (e.g. septic
shock) or when the results would change clinical management. Fever
is not always present when the patient has underlying infectious pa-
thology, and this pitfall is compounded by the poor sensitivity of oral
temperatures, especially in the elderly. In sum, fever is far from straight-
forward in its evaluation, and the EP must be diligent when deciding
how to pursue the etiology of fever.
Acknowledgements
No funds or grants were utilized for this clinical review. A prior,
shortened, extensively modified version was previously published on
emDocs.net. This review does not reflect the views or opinions of the
U.S. government, Department of Defense, U.S. Air Force, or SAUSHEC
EM Residency.
References
[1] Grandey KA. Fever [Internet]. In: Sherman SC, Weber JM, Schindlbeck MA, Rahul GP,
editors. Clinical emergency medicine. New York, NY: McGraw-Hill Education; 2014
([cited 2017 Jun 5] Available from:) accessemergencymedicine.mhmedical.com/
content.aspx?aid=1101224926.
[2] Morris F, Fletcher A. ABC of emergency differential diagnosis [Internet]. West Sussex, UK:
Blackwell Publishing; 2016([cited 2016 Nov 9] Available from:) https://www.google.
com/search?client=safari&rls=en&q=Fletcher_C000.indd+-
+ABC+Of+Emergency+Differential+Diagnosis+2009.pdf&ie=UTF-8&oe=UTF-8.
[3] Dinarello CA, Porat R. Fever [Internet]. In: Kasper D, Fauci A, Hauser S, Longo D,
Jameson JL, Loscalzo J, editors. Harrison's principles of internal medicine. 19e. New
York, NY: McGraw-Hill Education; 2015 ([cited 2016 Oct 29] Available from:)
http://mhmedical.com/content.aspx?aid=1120874671.
[4] Bleekers-Rovers C, van der Meer J, Beeching N. Fever. Medicine (Baltimore) 2009;
37(1):28–34.
[5] Young P, Saxena M, Bellomo R, et al. Acetaminophen for fever in critically ill patients
with suspected infection. N Engl J Med 2015;373(23):2215–24.
[6] Harrison M. Erythrocyte sedimentation rate and C-reactive protein. Aust Prescr
2015;38(3):93–4.
[7] Povoa P. C-reactive protein: a valuable marker of sepsis. Intensive Care Med 2002;
28:235–43.
[8] Pepys MB, Hirschfeld GM. C-reactive protein: a critical update. J Clin Invest 2003;
111:1805–12.
[9] Povoa P, Salluh JI. Biomarker-guided antibiotic therapy in adult critically ill patients:
a critical review. Ann Intensive Care 2012;2:32.
[10] Lee CC, Hong MY, Lee NY, et al. Pitfalls in using serum C-reactive protein to predict
bacteremia in febrile adults in the ED. Am J Emerg Med 2012;30(4):562–9.
[11] Erlinger TP, Platz EA, Rifai N, et al. C-reactive protein and the risk of incident colorec-
tal cancer. JAMA 2004;291(5):585–90.
[12] Musunuru K, Kral BG, Blumenthal RS, et al. The use of high-sensitivity assays for C-
reactive protein in clinical practice. Nat Clin Pract Cardiovasc Med 2008;5:621–35.
[13] Li K, Wei P, Qin Y, Wei Y. Is C-reactive protein a marker of obstructive sleep apnea?:
a meta-analysis. Medicine [serial online] May 2017;96(19):e6850 ((Available from:
MEDLINE with full text, Ipswich, MA). [Accessed 18 June 2017]).
[14] Lee S, Chan R, Wu J, Chen H, et al. Diagnostic value of procalcitonin for bacterial in-
fection in elderly patients - a systemic review and meta-analysis. Int J Clin Pract [se-
rial online] December 2013.
[15] Becker KL, Snider R, Nylen ES. Procalcitonin assay in systemic inflammation, infec-
tion, and sepsis: clinical utility and limitations. Crit Care Med 2008;36(3):941–52.
[16] Mat-Nor MB, Ralib A, Abdulah NZ, et al. The diagnostic ability of procalcitonin and
interleukin-6 to differentiate infectious from noninfectious systemic inflammatory
response syndrome and to predict mortality. J Crit Care 2016;33:245–51.
[17] Schuetz P, Muller B, Christ-Cran M, Stolz D, et al. Procalcitonin to initiate or discon-
tinue antibiotics in acute respiratory tract infections. Cochrane Database Syst Rev
2012 Sep 12;9:CD007498.
[18] Puskarich MA, Jones AE. Sepsis [Internet]. In: Tintinalli JE, Stapczynski JS, Ma OJ, Yealy DM,
Meckler GD, Cline DM, editors. Tintinalli's Emergency Medicine: A Comprehensive Study
Guide. 8e. New York, NY: McGraw-Hill Education; 2016 ([cited 2016 Nov 9] Available
from:) http://mhmedical.com/content.aspx?aid=1121510693.
[19] Fu CM, Tseng WP, Chiang WC, et al. Occult Staphylococcus aureus bacteremia in adult
emergency department patients: rare but important. Clin Infect Dis 2012 Jun;
54(11):1536–44.
[20] Makam AN, Auerbach AD, Steinham MA. Blood culture use in the emergency depart-
ment in patients hospitalized for community-acquired pneumonia. JAMA Intern
Med 2014;174(5):803–6.
[21] Benenson RS, Kepner AM, Pyle 2nd DN, Cavanaugh S. Selective use of blood cultures
in emergency department pneumonia patients. J Emerg Med 2007 Jul;33(1):1–8.
[22] Niven DJ, Gaudet JE, Laupland KB, et al. Accuracy of peripheral thermometers for es-
timating temperature: a systematic review and meta-analysis. Ann Intern Med
2015;163(10):768–77.
[23] McGugan EA. Hyperpyrexia in the emergency department. Emerg Med 2001;13(1):
116.
[24] Wester AL, Dunlop O, Melby KK, et al. Age-related differences in symptoms, diagno-
sis and prognosis of bacteremia. BMC Infect Dis 2013;13:346.
[25] Hernández C, Fehér C, Martínez J, et al. Clinical characteristics and outcome of elderly pa-
tients with community-onset bacteremia. J Infect [serial online] February 1, 2015;70:
135–43 ((Available from: ScienceDirect, Ipswich, MA). [Accessed 17 July 2017]).
[26] Fernandes D, Gonçalves-Pereira J, Janeiro S, et al. Acute bacterial meningitis in the
intensive care unit and risk factors for adverse clinical outcomes: retrospective
study. J Crit Care 2014;29(3):347–50.
[27] Caterino JM, Jalbuena T, Bogucki B. Predictors of acute decompensation after admis-
sion in ED patients with sepsis. Am J Emerg Med 2010;28(5):631–6.
[28] Burlaud A, Mathieu D, Falissard B, et al. Mortality and bloodstream infections in ge-
riatrics units. Arch Gerontol Geriatr 2010;51(3):e106-.
[29] Sunden-Cullberg J, Rylance R, Svefors J, et al. Fever in the emergency department
predicts survival of patients with severe sepsis and septic shock admitted to the
ICU. Crit Care Med 2017;45(4):591–9.
[30] Raith EP, Udy AA, Bailey M, et al. Prognostic accuracy of the SOFA score, SIRS criteria,
and qSOFA score for in-hospital mortality among adults with suspected infection ad-
mitted to the intensive care unit. JAMA 2017;317(3):290–300.
[31] Nucifora G, Badano L, Hysko F, et al. Pulmonary embolism and fever. Circulation
2007;115(6):e173-.
[32] Stein PD, Willis III PW, DeMets DL. History and physical examination in acute pul-
monary embolism in patients without preexisting cardiac or pulmonary disease.
Am J Cardiol 1981;47:218–23.
[33] Murray HW, Ellis GC, Blumenthal DS, et al. Fever and pulmonary thromboembolism.
Am J Med 1979;67:232–5.
[34] Stein PD, Afzal A, Henry JW, et al. Fever in acute pulmonary embolism. Chest 2000;
117(1):39–42.
[35] Calvo-Romero JM, Lima-Rodríguez EM, Pérez-Miranda M, et al. Low-grade and high-
grade fever at presentation of acute pulmonary embolism. Blood Coagul Fibrinolysis
Int J Haemost Thromb 2004;15(4):331–3.