Postoperative fever

Authors:
Harrison G Weed, MS, MD, FACP
Larry M Baddour, MD, FIDSA, FAHA
Section Editor:
Hilary Sanfey, MD
Deputy Editor:
Kathryn A Collins, MD, PhD, FACS

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Jan 2018. | This topic last updated: Jan 11, 2018.

INTRODUCTION — Fever above 38ºC (100.4ºF) is common in the first few days after
major surgery [1,2]. Most early postoperative fever is caused by the inflammatory stimulus
of surgery and resolves spontaneously [3-7]. However, postoperative fever can be a
manifestation of a serious complication.

A thorough differential diagnosis of postoperative fever includes infectious and

noninfectious conditions that occur following surgery. Fever may arise due to a surgical
site infection (SSI), or from other hospital-related conditions, including nosocomial
pneumonia, urinary tract infection, drug fever, and deep vein thrombosis (table 1). In
evaluating a postoperative patient with fever, it is important to consider a broad differential,
and not to assume that fever is due to infection.

Fever as a manifestation of infection may be reduced or absent in immunocompromised

patients, including those receiving glucocorticoids, cancer chemotherapy, post-transplant
immunosuppression, and also in some patients who are elderly or have chronic renal
failure.

The evaluation of fever in immunocompromised patients is discussed elsewhere.

(See "Fever and rash in immunocompromised patients without HIV
infection" and "Approach to the immunocompromised patient with fever and pulmonary
infiltrates" and "Overview of neutropenic fever syndromes" and "Diagnostic approach to
the adult cancer patient with neutropenic fever".)

PATHOPHYSIOLOGY OF POSTOPERATIVE FEVER — Fever is a manifestation of

cytokine release in response to a variety of stimuli [8-10]. Fever-associated cytokines,
including interleukin (IL)-1, IL-6, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-
gamma, are produced by a variety of tissues and cells (algorithm 1). There is some
evidence that IL-6 is the cytokine most closely correlated with postoperative fever [11].
(See "Pathophysiology and treatment of fever in adults".)
Fever-associated cytokines are released by tissue trauma and do not necessarily signal
infection. The magnitude of the trauma is correlated with the degree of the fever response.
For example, laparoscopic cholecystectomy is associated with less tissue trauma and
fewer episodes of postoperative fever than is open cholecystectomy [12]. Similarly, there is
less postoperative fever when coronary artery grafting is performed without the use of a
cardiopulmonary bypass pump [13].

Genetic factors may influence the magnitude of the cytokine release in response to tissue
trauma and thus the magnitude of self-limited postoperative fever. For example, children
with osteogenesis imperfecta undergoing orthopedic surgery appear to have a greater and
more sustained febrile response than matched controls [14].

Bacterial endotoxins and exotoxins can stimulate cytokine release and cause
postoperative fever. Bacteria or fragments of bacteria translocated from the colon (eg, as a
consequence of perioperative ileus or hypotension) may be responsible for some episodes
of self-limited postoperative fever. Elevated levels of bacterial DNA have been
demonstrated with polymerase chain reaction (PCR) testing of blood from surgical
patients, even in patients whose blood cultures are negative [15].

Nonsteroidal anti-inflammatory agents (NSAIDs) and glucocorticoids suppress cytokine

release and thereby reduce the magnitude of the febrile response [16,17].

TIMING OF FEVER — The timing of fever after surgery is one of the most important
factors to consider in generating a prioritized differential diagnosis of postoperative fever
(figure 1). The timing of postoperative fever can be usefully described as:

●Immediate – Onset in the operating suite or within hours after surgery

●Acute – Onset within the first week after surgery

●Subacute – Onset from one to four weeks following surgery

●Delayed – Onset more than one month after surgery

Immediate — The potential causes of fever in the immediate operative and postoperative
period are mainly limited to medications or blood products to which the patient was
exposed during perioperative care either in the operating room or in the recovery area,
trauma suffered prior to surgery or as part of surgery, infections that were present prior to
surgery, and, rarely, malignant hyperthermia.

Adverse medication reactions that produce immediate fever include immune-mediated

reactions, such as reactions to antimicrobials and to transfused blood products. The
vasodilation that often accompanies these reactions makes hypotension a common
presenting sign; rash may accompany fever in some patients with medication reactions.
(See "Drug fever".)
The initial clinical signs (ie, hypercarbia) of malignant hyperthermia typically present within
30 minutes following the administration of a triggering agent (eg, inhaled
anesthetics, succinylcholine) but have been reported later in the operative course and also
following cessation of anesthesia. If the malignant hyperthermia response is not
recognized and aborted with dantrolene, high fever may develop as a result of
hypermetabolism. (See "Malignant hyperthermia: Clinical diagnosis and management of
acute crisis".)

Fever due to the trauma of surgery usually resolves within two to three days. The severity
and duration of these self-limited postoperative fevers depends on the type of surgery
[18,19] but tends to be greater in patients with longer and more extensive surgical
procedures [12]. Fever caused by severe head trauma can be persistent and may resolve
gradually over days or even weeks [20].

Acute — There are many causes of fever in the first week after surgery. Nosocomial
infections are common during this period. Occasionally, fever or other symptoms predate
surgery and are manifestations of community-acquired infection, such as a viral upper
respiratory tract infection.

While surgical site infection (SSI) and intravascular catheter infections can cause acute
postoperative fever, other infections are more frequently identified, including pneumonia
and urinary tract infection (UTI).

●Patients receiving mechanical ventilation during surgery are at risk for ventilator-
associated pneumonia (VAP). The risk of VAP increases with the duration of
mechanical ventilation [21]. The risk of pneumonia tapers to a stable, lower rate over
the first postoperative week and with the discontinuation of mechanical ventilation.
(See "Clinical presentation and diagnostic evaluation of ventilator-associated
pneumonia".)

●Patients with depressed mental status or gag reflex due to anesthesia and analgesia
are more susceptible to aspiration if they vomit after surgery. A nasogastric tube also
increases gastroesophageal reflux and the risk for aspiration [22]. (See "Aspiration
pneumonia in adults".)

●UTI is a frequent cause of postoperative fever in patients with indwelling urethral

catheters. The risk of UTI increases with the duration of catheterization [23,24]. UTI is
more common in patients who have undergone a genitourinary procedure and in
those who have chronic, indwelling catheters prior to surgery. (See "Catheter-
associated urinary tract infection in adults".)

●SSI most often presents in the subacute period, one week or more after surgery.
However, two organisms, group A streptococcus (GAS) and Clostridium perfringens,
can cause fulminant SSI within a few hours after surgery. (See "Necrotizing soft
tissue infections" and "Clostridial myonecrosis".)
 ●Catheter exit site infections and bacteremia associated with intravascular catheters
also tend to occur subacutely but should be considered as sources of fever in any
patient with a catheter in place, especially if insertion was performed under emergent
or nonsterile conditions. (See "Epidemiology, pathogenesis, and microbiology of
intravascular catheter infections".)

Acute fever can also be caused by noninfectious conditions. Pancreatitis, myocardial

infarction, pulmonary embolism, thrombophlebitis, alcohol withdrawal, and acute gout can
complicate the acute postoperative period.

Subacute — SSI is a common cause of fever more than one week after surgery; many
patients have already been discharged from the hospital by this time [25-28].
(See "Complications of abdominal surgical incisions".)

Central venous catheters, if used, can be a source of infection and fever.

(See "Epidemiology, pathogenesis, and microbiology of intravascular catheter infections".)

Fever from antibiotic-associated diarrhea, typically attributed to Clostridium difficile, also

occurs more commonly during this period. (See "Clostridium difficile in adults:
Epidemiology, microbiology, and pathophysiology".)

Febrile drug reactions are a frequent cause of subacute fever. Beta-lactam antibiotics and
sulfa-containing products are commonly implicated, but other medications, such as H2-
blockers, procainamide, phenytoin, and heparin, should be considered.

Thrombophlebitis should be considered as a cause of subacute fever in a patient with

impaired mobility. Deep venous thrombosis and pulmonary embolism can cause fever and
are more frequent in patients who are debilitated either by chronic medical problems or by
the surgery.

Patients who require critical care after surgery are at higher risk for the development of
subacute fever [29]. These patients typically develop a variety of postoperative
complications. Nosocomial infections are more common in these patients because of their
treatment with invasive medical devices. Device-related infections due to bacteria and
fungi include intravascular catheter-related infection with or without bacteremia, VAP, UTI,
and sinusitis. (See "Infections and antimicrobial resistance in the intensive care unit:
Epidemiology and prevention".)

Delayed — Most delayed postoperative fevers are due to infection, although fever due to
postpericardiotomy syndrome should be considered in patients following cardiac surgery.

Viral infections from blood products, including cytomegalovirus (CMV), hepatitis viruses,
and human immunodeficiency virus (HIV), can arise late in postoperative patients [13].
Parasitic infections (eg, toxoplasmosis, babesiosis, Plasmodium malariae infection) can
also rarely be transmitted via transfusion [30-33].
SSIs due to more indolent microorganisms (eg, coagulase-negative staphylococci) can
cause delayed fever, especially in patients with implanted medical devices or grafts.
(See "Epidemiology, pathogenesis, and microbiology of intravascular catheter
infections" and "Diagnosis of intravascular catheter-related infections".)

Patients can also develop delayed cellulitis when surgery has disrupted venous or
lymphatic drainage; this type of cellulitis can be recurrent [34,35]. (See "Cellulitis following
pelvic lymph node dissection" and "Breast cellulitis and other skin disorders of the
breast" and "Early noncardiac complications of coronary artery bypass graft surgery",
section on 'Post-venectomy cellulitis'.)

Infective endocarditis due to perioperative bacteremia is also more likely to present weeks
or months after surgery.

CAUSES OF POSTOPERATIVE FEVER — Although the list of causes of postoperative

fever is extensive (table 1), the initial focus for most patients should be on a limited
number of the more common infectious and noninfectious causes.

Infectious — SSI, pneumonia (especially VAP), UTI, and intravascular catheter-

associated infection are the most common infectious causes of postoperative fever.
Nosocomial bacterial and fungal pathogens are usually implicated. The infecting
microorganisms generally are found as endogenous flora of the skin or bowel, but the flora
change as patients are hospitalized for longer periods and receive antimicrobial therapy.

When patients are readmitted to the hospital, organisms acquired in the community may
also be involved. As an example, Pasteurella multocida SSIs have been caused by pet
cats and dogs licking a surgical site [36].

Viral infections in the postoperative patient are usually associated with the transfusion of
blood products. However, blood for transfusion is routinely screened for only a discrete
number of agents (table 2). Donated blood is screened by immunoassay techniques for a
number of viruses (eg, HIV, human T-lymphotropic virus [HTLV], hepatitis C, hepatitis B,
cytomegalovirus [CMV], Zika). Other infective agents may be transmitted and cause fever
in the postoperative period. As an example, Babesia is screened for only by questioning
potential blood donors. Transfusion-related babesiosis was responsible for 4 of the 15
transfusion-related deaths in the United States in 2014 [37]. (See "Blood donor screening:
Laboratory testing", section on 'Infectious disease screening' and "Blood donor screening:
Laboratory testing", section on 'Emerging infectious disease agents'.)

Viral infections in the postoperative patient can also be transmitted nosocomially, as has
occurred with severe acute respiratory syndrome (SARS) [38]. Finally, postoperative viral
infections such as VAP can occasionally be caused by the reactivation of latent viruses,
such as CMV or herpes simplex virus (HSV), especially in immunosuppressed patients
[39-41].
Other postoperative infections include [42]:

●Sinusitis and, less commonly, otitis media, especially in patients with nasotracheal
or nasogastric tubes. Mild sinusitis in a critically ill patient may not be clinically
significant [43,44].

●Bacterial meningitis in patients after neurosurgical or head and neck procedures that
inadvertently violated the subarachnoid space causing a "CSF leak."

●Parotitis, usually due to Staphylococcus aureus, in patients who have undergone

manipulation of the oral cavity or who are significantly dehydrated postoperatively.
This postoperative infection is far less frequent with modern anesthesia and
perioperative care [45].

●Acalculous cholecystitis can occur as a postoperative infection, and recent surgery

is second only to trauma as a cause of this complication [46].

●Toxic shock syndrome is uncommon but can occur, particularly in patients with
nasal or vaginal packing that may facilitate the growth of S. aureus or GAS [47,48].
(See "Staphylococcal toxic shock syndrome" and "Epidemiology, clinical
manifestations, and diagnosis of streptococcal toxic shock syndrome".)

Noninfectious — Noninfectious causes of postoperative fever include underlying

conditions that are unmasked by the stress of surgery (table 1). Other causes to be
considered are:

Medication — Medications are the most common noninfectious cause of fever.

Antimicrobials and heparin are the medications most commonly associated with
postoperative fever, at least in part because they are used so frequently in the
postoperative period (table 3). (See "Drug fever".)

Several medications commonly used in the postoperative period can interact with selective
serotonin reuptake inhibitors (SSRIs) or other antidepressants to precipitate fever as one
manifestation of the serotonin syndrome. (See "Selective serotonin reuptake inhibitors:
Pharmacology, administration, and side effects", section on 'Drug-drug interactions'.)

Additionally, antimicrobials and other medications incorporated into implanted materials

may cause postoperative fever [49].

Malignant hyperthermia — Malignant hyperthermia (MH) is an inherited disorder most

commonly manifesting as hypermetabolism during general anesthesia. MH-susceptible
patients have genetic skeletal muscle receptor abnormalities allowing excessive calcium
accumulation in the presence of certain anesthetic triggering agents. Prompt recognition of
the initial clinical signs and treatment with dantrolene limits the morbidity and mortality
associated with this disorder. (See "Susceptibility to malignant hyperthermia: Evaluation
and management" and "Malignant hyperthermia: Clinical diagnosis and management of
acute crisis".)

Inflammation — Surgical site inflammation without infection, including seroma and

hematoma.

Pyoderma gangrenosum, although rare in the postoperative period, is an ulcerative

inflammatory skin disorder that can mimic wound infection [50]. It is important to make the
distinction, as treatment for pyoderma is glucocorticoid therapy, not antibiotics.

Various cutaneous drug reactions (eg, acute generalized exanthematous pustulosis, the
DRESS [drug reaction with eosinophilia and systemic symptoms] syndrome, cutaneous
small vessel vasculitis), cause inflammatory changes in the skin and may be associated
with fever [51]. (See "Drug eruptions".)

Gout — Gout and pseudogout in association with joint inflammation and effusion [52,53].
Oncologic surgery or concomitant cancer may be additional risk factors for postoperative
gout and joint manipulation and hyperparathyroidism for pseudogout. (See "Clinical
manifestations and diagnosis of gout" and "Clinical manifestations and diagnosis of
calcium pyrophosphate crystal deposition (CPPD) disease".)

Pancreatitis — Pancreatitis can result from surgery involving the upper abdomen [54], an
adverse reaction to perioperative medications, or preoperative alcoholism. (See "Etiology
of acute pancreatitis".)

Deep venous thrombosis — Deep vein thrombosis (DVT) and pulmonary embolization
are more common after procedures either directly or indirectly resulting in venous stasis,
such as oncologic, pelvic, orthopedic, and neurosurgeries. (See "Overview of the causes
of venous thrombosis", section on 'Surgery' and "Overview of the causes of venous
thrombosis", section on 'Trauma'.)

Fat embolism — Fat embolism occurs most frequently after surgeries for major blunt
trauma or major orthopedic surgery (particularly those involving long bone and pelvic
fractures) [55-58]. It can also develop after liposuction [59] and is part of the differential
diagnosis in postoperative patients suffering from acute sickle cell chest syndrome [60].
(See "Fat embolism syndrome".)

Cardiovascular and stroke — Myocardial infarction, stroke, and subarachnoid

hemorrhage can cause postoperative fever [61-63].

Transfusion reaction — Transfusion reactions, such as delayed serologic and hemolytic

transfusion reactions (DSTRs, DHTRs), are more common in patients previously
sensitized to foreign antigens through prior transfusion or multiple pregnancies [64].
(See "Immunologic transfusion reactions".)
Complement activation due to antibody incompatibilities can also cause acute lung injury
in the syndrome of transfusion-related acute lung injury (TRALI) [65]. (See "Transfusion-
related acute lung injury (TRALI)".)

Endocrine — Hyperthyroidism or thyroid storm can occasionally cause postoperative

fever. Although hyperthyroidism is more common in patients undergoing thyroid or other
neck surgeries, it can also occur after other surgeries [66-68]. Acute adrenal insufficiency
or Addisonian crisis has also been reported to occur after surgery, usually due to bilateral
adrenal hemorrhagic infarction from coagulopathy [69,70]. The diagnosis can be obscure
but is important because treatment with glucocorticoids can be lifesaving [71,72].
(See "Clinical manifestations of adrenal insufficiency in adults".)

Atelectasis (not causal) — Atelectasis is often used as an explanation for otherwise

unexplained postoperative fever. Both atelectasis and fever occur frequently after surgery,
but their concurrence is probably coincidental rather than causal. (See "Atelectasis: Types
and pathogenesis in adults".)

●In one study of 270 consecutive patients after abdominal surgery, the sensitivity and
negative predictive value of fever as a predictor of atelectasis were both less than 50
percent, and the specificity and positive predictive value were 68 and 66 percent
respectively [73].

●In another study, there was also no association between fever and the presence of,
or the degree of, atelectasis [74]. Therefore, ascribing a postoperative fever to
atelectasis is probably false reassurance and may mislead the clinician from pursuing
the true cause of the fever.

Neuroleptic malignant syndrome — Neuroleptic malignant syndrome causing high fever

and rigidity can develop perioperatively in patients receiving antipsychotic agents,
especially haloperidol [75]. (See "Neuroleptic malignant syndrome".)

CONSIDERATIONS FOLLOWING SPECIFIC SURGERIES

Cardiothoracic surgery — Fever is common in the first few days after cardiothoracic
surgery; additional investigation in febrile but otherwise clinically unremarkable
postoperative patients is probably not indicated until the third postoperative day [76,77].
Individual indicators of infection, including fever, are unreliable in the immediate
postoperative period. Aggregate measures of physiologic instability such as a persistently
poor APACHE score can identify patients more likely to have serious infectious
complications [78]. (See "Predictive scoring systems in the intensive care unit", section on
'Acute Physiologic and Chronic Health Evaluation (APACHE)'.)

Pneumonia is a common cause of fever after cardiac surgery and may occur in more than
5 percent of patients [79]. Pneumonia is correlated with reintubation, hypotension,
neurologic dysfunction, and transfusion of more than three units of blood components [79].
Pleural effusions are the rule in patients following cardiac surgery; thoracentesis is rarely
required during the evaluation of fever in such patients.

Sternal wound infection and mediastinitis — Sternal wound infection occurs in

approximately 1 percent of patients after median sternotomy with a median time to
infection of 20 days in a multi-institutional cohort study [80]. Sternal wound infection more
than one month after surgery is unusual (only 9 percent in another study [81]).
Mediastinitis is associated with significant mortality (14 to 47 [82-86]) and causes
protracted hospitalization and an increased need for reoperation and rehospitalization.
(See "Postoperative mediastinitis after cardiac surgery"and "Surgical management of
sternal wound complications".)

A positive blood culture in a persistently febrile patient can be the first manifestation of a
sternal wound infection, occurring before apparent wound inflammation [87]. Risk factors
for sternal wound infection include surgeries that are emergent, longer, more complex, or
include internal mammary artery grafting, and patients who are older, diabetic, dialysis
dependent, obese, or smoke [27,88-91]. Endocarditis should be considered in patients
who develop positive blood cultures after undergoing valve replacement.
(See "Epidemiology, clinical manifestations, and diagnosis of prosthetic valve
endocarditis".)

Culture of Staphylococcus aureus from the blood raises the possibility of mediastinitis,
even if the wound appears uninfected [92,93] (see "Postoperative mediastinitis after
cardiac surgery"). Recovery of organisms other than S. aureus from blood cultures,
however, does not appear to be associated with mediastinitis. One study found that among
patients who had undergone coronary artery bypass graft surgery and had blood cultures
that grew an organism other than S. aureus, only 12 percent developed mediastinitis [93].
Coagulase-negative staphylococci are another common cause of sternal wound infections;
sternal wound infections due to these organisms are often clinically less apparent than
those due to S. aureus [87,88,94]. Sternal wound dehiscence without apparent infection is
a clue for infection due to coagulase-negative staphylococci [94].

Candida species account for most postoperative fungal infections,

but Aspergillus infections also occur [95]. Aspergillus infections usually present months to
years after surgery with persistent fever and negative blood cultures and a mortality rate
greater than 80 percent. To minimize the risk of postoperative Aspergillus infection and its
associated morbidity and mortality, it is critical to maintain hospital surveillance and to
investigate and address any apparent outbreaks [96].

An important noninfectious cause of fever after cardiothoracic surgery is the

postpericardiotomy syndrome, which can present days to weeks after surgery with fatigue
and chest pain, with or without pericardial effusion [61,97]. (See "Post-cardiac injury
syndromes".)
Neurosurgery — Meningitis is a frequent and serious cause of fever after neurosurgery
[98]. Classic symptoms and signs of meningeal inflammation, such as headache,
photophobia, and nuchal rigidity, are usually not helpful because they can be caused
either by infection or by hemolyzed blood from the surgery irritating the meninges.
Microscopic and analytical examination of the cerebrospinal fluid (CSF) is indicated in
patients with fever, because, combined with specific clinical findings, characteristics of the
CSF can help to distinguish patients with infections from those with chemical meningitis.
Patients with all of the following criteria can probably be safely observed without
administration of antimicrobials: fever less than 39.4ºC (102.9ºF); CSF white blood count
(WBC) less than 7,500/microL; CSF glucose above 10 mg/dL; no delirium, seizure, or
surgical site inflammation [99]. Measurement of CSF lactate might be useful in
distinguishing bacterial meningitis from those with chemical meningitis in neurosurgery
patients [100,101].

Neurosurgical procedures that impact the hypothalamus can lead to disorders of

thermoregulation and cause postoperative fever [102].

Deep vein thrombosis (DVT) occurs more frequently after neurosurgery than after many
other types of surgery. Not only is the patient likely to have limited mobility before and after
surgery, but prophylactic anticoagulation is often less aggressive for neurosurgery
because of concern for central nervous system hemorrhage.

Vascular surgery — Graft infections after vascular surgery may occur by direct
inoculation of the surgical site or, less frequently, by hematogenous spread. Infection is
more common in grafts at inguinal and upper leg surgical sites. Vascular graft infections
most commonly present soon after surgery but can occur months to years later.

Determining that a graft is infected can be difficult. In addition to systemic symptoms such
as fatigue, and anorexia, and signs such as fever, imaging with computed tomography
(CT) scanning, magnetic resonance (MR) imaging, or scintigraphy can be helpful.
Negative findings on imaging studies do not rule out a graft infection, but positive findings
help to confirm infection and to guide aspiration for microbiologic analysis.

In patients who undergo endovascular repair of aortic aneurysms with endoluminal stent-
grafts, a syndrome has been described that can include fever, leukocytosis, elevated C-
reactive protein levels, and perigraft gas seen radiographically. Fever above 101.4ºF
(38.6ºC) has been reported in up to two-thirds of patients in some series. Blood cultures
are negative, and the fevers resolve without antimicrobial therapy [103,104]. This is
sometimes referred to as "postimplantation syndrome"; its cause is uncertain [105,106].
(See "Complications of endovascular abdominal aortic repair", section on 'Postimplantation
syndrome'.)

Another noninfectious cause of fever after vascular surgery is arterial embolization, or

"blue toe" syndrome. A similar syndrome can be caused by emboli from an infected graft.
Abdominal surgery — The primary cause of postoperative fever that is unique to
abdominal surgery is deep abdominal abscess. Distinguishing between abscess,
hematoma, and a benign peritoneal fluid collection can be difficult. Imaging studies and
needle aspiration may be helpful, but exploration is sometimes necessary. Empiric
antimicrobial treatment should be directed at the combination of aerobic Gram-negative
enteric bacilli and anaerobes.

Splenoportal thrombosis may cause fever following splenectomy, and is recognized with
increased frequency since the availability of CT scanning [107]. Risk factors include
massive splenomegaly and myeloproliferative and hemolytic disorders.

Pancreatitis more frequently causes postoperative fever after upper abdominal surgeries
than after other surgeries. Diagnosis can be made by elevated serum amylase and lipase
concentrations with the considerations that salivary glands also produce amylase, and
macro variants of amylase can produce elevated serum concentrations. (See "Clinical
manifestations and diagnosis of acute pancreatitis".)

Obstetric and gynecologic surgery — Postpartum endometritis, manifested by fever,

pelvic pain and purulent vaginal discharge, is more common in patients with preexisting
medical problems, after premature rupture of membranes, difficult deliveries, and after the
use of internal fetal monitoring. (See "Postpartum endometritis".)

The differential diagnosis of fever after gynecologic surgery includes urinary tract infection
(UTI), cellulitis, necrotizing fasciitis, superficial abscess, deep abscess, and pelvic
thrombophlebitis. As with other major surgeries, fever in the first day or two after
gynecologic surgery usually resolves spontaneously. Extensive laboratory testing is not
beneficial; fever evaluation should be targeted to the individual patient, based on repeated
assessment of symptoms and signs [108,109].

Deep abscess and pelvic thrombophlebitis are possible causes in patients with an
unrevealing evaluation and persistent fever. Similar to abdominal surgery, identifying a
fluid collection and distinguishing between abscess, hematoma, and a benign fluid
collection, though difficult, can be critically important.

Urologic surgery — Infection of the urinary tract at any level is the major consideration in
evaluating patients with fever after urologic surgery. Although bacteriuria due to a urethral
catheter is common, culture alone is not as revealing as the combination of urine culture
findings and urine analysis for pyuria and bacteriuria. Deep infections, such as prostatic
and perinephric abscess, may present with fever and pain but relatively benign urine
findings. Infection can also spread from the lower urinary tract through Batson's venous
plexus to the lumbar spine and present after the urinary tract infection is resolved.
(See "Catheter-associated urinary tract infection in adults".)

Orthopedic surgery — As with other major surgeries, self-limited fever is the rule after
major orthopedic surgery [6]. The dominant special considerations in the differential
diagnosis of persistent fever are surgical site infection, infected prosthesis, hematoma, and
deep vein thrombosis. Repeat clinical assessment, imaging, and sometimes needle
aspiration may be required to adequately assess the surgical site.

Transplantation — Evaluating fever after transplantation surgery requires special

considerations due to immunosuppression [110,111]. In addition to usual bacterial
infections, medication reactions, and DVT, immunosuppression can enable reactivation of
viral and protozoan infections from the patient or the donor [112]. In addition, organ
rejection and immunosuppression-related lymphoma are both associated with delayed
fever. Finally, immunosuppressive medications such as corticosteroids can mask fever.

APPROACH TO THE PATIENT WITH FEVER AFTER SURGERY — Chest radiography,

urinalysis, and blood and urine cultures are notindicated for all postoperative patients with
fever. The need for laboratory testing should be determined by the findings of a careful
history and physical examination. The febrile postoperative patient should be evaluated
systematically (table 4), taking into account the timing of the onset of fever and the many
possible causes (table 1) [7,108,113].

A useful initial screen for the more common causes of postoperative fever is represented
by the following mnemonic, the order of which implies the timing of postoperative fever:

●"Wind" refers to pulmonary causes of fever, including pneumonia, aspiration, and

pulmonary embolism (but not atelectasis).

●"Water" refers to urinary tract infection.

●"Wound" refers to surgical site infection.

●"Walking" refers to thromboembolism.

●"Wonder drugs" refers to drug-related fever.

●"What did we do?" is a reminder to consider treatments as a cause of fever and

includes medications, blood product transfusions, and intravascular, urethral, nasal,
and abdominal catheters.

Procalcitonin — The value of serum procalcitonin (PCT) concentration for differentiating

bacterial infection from other causes of postoperative fever has been explored in a few
studies [114-116]. PCT is produced in C cells of the thyroid and is a more specific marker
of bacterial infection than CRP. However, postoperative PCT concentrations vary
substantially following different types of surgery [116], and from patient to patient following
the same type of surgery [117]. Furthermore, PCT has not been found to be a reliable
marker for infection in other settings (see "Fever in the intensive care unit" and "Evaluation
and management of suspected sepsis and septic shock in adults"). We do not suggest the
use of PCT in the evaluation of postoperative fever, pending additional clinical evidence.
TREATMENT — Any unnecessary treatments, including medications and catheters,
should be discontinued in patients with postoperative fever. It is probably appropriate to
suppress the fever in most patients with one or two days of scheduled acetaminophen to
minimize patient discomfort and the physiologic stress and metabolic demands of fever
and shivering [118]. This approach is unlikely to mask a significant pathologic condition.
Additional treatment depends upon the cause of the fever.

The decision to administer antibiotics to a patient with postoperative fever depends upon
careful clinical assessment including an appraisal of the patient's stability. Moreover, it is
important to highlight that most cases of postoperative fever are due to noninfectious
causes. Patients who have undergone major surgery and are receiving intensive care and
patients with hemodynamic instability generally should be treated empirically with broad-
spectrum antibiotics after cultures have been obtained. As an example, a patient with a
suspected intra-abdominal or pelvic infection should be treated with a regimen effective
against aerobic Gram-negative enteric bacilli and anaerobes. Empiric antifungal therapy
should not be included unless the patient is at high risk for fungal infection.

Nosocomial pathogens are often resistant to many antimicrobials; hospital antibiograms

can be useful for selecting an appropriate broad-spectrum regimen. If a source of fever is
not apparent and blood cultures show no growth after 48 hours, then discontinuation of
antimicrobials should be seriously considered.

If a site of infection is identified and/or cultures are positive, the broad-spectrum regimen
should be focused to cover the probable or known causative organism(s). Antimicrobial
treatment beyond the empiric period of 48 hours should be reserved for patients in whom
an infection has been identified. Gram stain findings and hospital antibiograms can be
used to guide empiric antimicrobial selection, but definitive treatment should be based
upon antimicrobial susceptibility results from cultured organisms. Carefully selecting
antimicrobial treatment can help to avoid adverse medication reactions and can help to
minimize the prevalence of resistant organisms in the hospital.

SUMMARY AND RECOMMENDATIONS

●Postoperative fever (>38°C, 100.4°F) is common in the first few days after surgery
and usually resolves spontaneously. This febrile response may be due to tissue
trauma with cytokine release, circulating bacterial endotoxins from endogenous gut
flora, or other causes. (See 'Pathophysiology of postoperative fever' above.)

●In establishing a differential diagnosis for postoperative fever, it is helpful to take into
account the timing of fever onset following surgery: immediate, acute, subacute, or
delayed. The differential diagnosis of postoperative fever includes infectious and
noninfectious etiologies. (See 'Timing of fever' above.)
●Surgical site infection, pneumonia, urinary tract infection, and intravascular catheter
infection are the predominant infectious causes of postoperative fever and are often
due to nosocomial multi-drug-resistant organisms. (See 'Infectious' above.)

●The most common noninfectious cause of postoperative fever is a medication

reaction; antimicrobial agents or heparin are the drugs most frequently implicated.
(See 'Medication' above.)

●Atelectasis and fever can both occur after surgery; however, they do not correlate
well with each other. Although atelectasis is often cited as a cause of postoperative
fever, the association is probably coincidental and not causal. (See 'Atelectasis (not
causal)' above.)

●Fever occurring in a patient who is otherwise doing well clinically within two days
following cardiovascular surgery probably does not need further evaluation. A more
delayed fever can be due to a variety of causes. Pneumonia occurs in more than 5
percent of sternotomy patients, and sternal complications in 1 to 5 percent.
Mediastinitis is a serious complication and is usually due to Staphylococcus species.
The postpericardiotomy fever syndrome may occur weeks after surgery.
(See 'Cardiothoracic surgery' above.)

●Meningitis may be difficult to diagnose following neurosurgery, because

neurosurgery can cause meningeal irritation without infection. Cerebrospinal fluid
should be obtained for glucose concentration and microbiologic studies (gram stain
and bacterial culture) to help determine the need for empiric antimicrobial therapy.
(See 'Neurosurgery' above.)

●Vascular graft infections are more common after revascularization involving the
groin or lower extremities. In patients undergoing endovascular aortic aneurysm
repair, a postimplantation syndrome with fever but no infection is uncommon but has
been described. (See 'Vascular surgery' above.)

●Fever following abdominal surgery may be due to intra-abdominal abscess, and

exploration may be necessary if needle aspiration and imaging studies are
inconclusive. Pancreatitis more frequently complicates upper abdominal surgery than
other surgeries. (See 'Abdominal surgery' above.)

●Endometritis is more common following complicated deliveries. Fever soon after

pelvic surgery is most often transient but may be due to urinary tract infection,
cellulitis, abscess, or pelvic thrombophlebitis. (See 'Obstetric and gynecologic
surgery' above.)

●Fever evaluation in the post-transplant patient is complicated by the increased

likelihood of opportunistic infections due to concomitant immunosuppression.
(See 'Transplantation' above.)
 ●Chest X-ray, urinalysis, and blood cultures are not indicated for most febrile
postoperative patients. Evaluation should be tailored to the individual patient based
on history, symptoms, and physical findings. (See 'Approach to the patient with fever
after surgery' above.)

●All unnecessary treatments, including medications, nasogastric tubes, and

intravascular and urinary catheters should be discontinued in the febrile patient.
Treating the fever with acetaminophen is often appropriate. Antibiotics are not
routinely indicated for most patients with fever in the early postoperative period, but
hemodynamically unstable patients should be treated empirically with broad-spectrum
antibiotics, which should be discontinued after 48 hours if no source of infection has
been identified. (See 'Treatment' above.)

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

1. Garibaldi RA, Brodine S, Matsumiya S, Coleman M. Evidence for the non-infectious

etiology of early postoperative fever. Infect Control 1985; 6:273.
2. Galicier C, Richet H. A prospective study of postoperative fever in a general surgery
department. Infect Control 1985; 6:487.
3. Livelli FD Jr, Johnson RA, McEnany MT, et al. Unexplained in-hospital fever following
cardiac surgery. Natural history, relationship to postpericardiotomy syndrome, and a
prospective study of therapy with indomethacin versus placebo. Circulation 1978; 57:968.
4. Hobar PC, Masson JA, Herrera R, et al. Fever after craniofacial surgery in the infant under
24 months of age. Plast Reconstr Surg 1998; 102:32.
5. Guinn S, Castro FP Jr, Garcia R, Barrack RL. Fever following total knee arthroplasty. Am J
Knee Surg 1999; 12:161.
6. Ghosh S, Charity RM, Haidar SG, Singh BK. Pyrexia following total knee replacement.
Knee 2006; 13:324.
7. Kiragu AW, Zier J, Cornfield DN. Utility of blood cultures in postoperative pediatric
intensive care unit patients. Pediatr Crit Care Med 2009; 10:364.
8. Netea MG, Kullberg BJ, Van der Meer JW. Circulating cytokines as mediators of fever.
Clin Infect Dis 2000; 31 Suppl 5:S178.
9. Blatteis CM, Sehic E, Li S. Pyrogen sensing and signaling: old views and new concepts.
Clin Infect Dis 2000; 31 Suppl 5:S168.
10. Saper CB, Breder CD. The neurologic basis of fever. N Engl J Med 1994; 330:1880.
11. Mitchell JD, Grocott HP, Phillips-Bute B, et al. Cytokine secretion after cardiac surgery and
its relationship to postoperative fever. Cytokine 2007; 39:37.
12. Dauleh MI, Rahman S, Townell NH. Open versus laparoscopic cholecystectomy: a
comparison of postoperative temperature. J R Coll Surg Edinb 1995; 40:116.
13. Clark JA, Bar-Yosef S, Anderson A, et al. Postoperative hyperthermia following off-pump
versus on-pump coronary artery bypass surgery. J Cardiothorac Vasc Anesth 2005;
19:426.
14. Ghert M, Allen B, Davids J, et al. Increased postoperative febrile response in children with
osteogenesis imperfecta. J Pediatr Orthop 2003; 23:261.
15. Kane TD, Alexander JW, Johannigman JA. The detection of microbial DNA in the blood: a
sensitive method for diagnosing bacteremia and/or bacterial translocation in surgical
patients. Ann Surg 1998; 227:1.
16. Held BI, Michels A, Blanco J, Ascher-Walsh C. The effect of ketorolac on postoperative
febrile episodes in patients after abdominal myomectomy. Am J Obstet Gynecol 2002;
187:1450.
17. Bisgaard T, Klarskov B, Kehlet H, Rosenberg J. Preoperative dexamethasone improves
surgical outcome after laparoscopic cholecystectomy: a randomized double-blind placebo-
controlled trial. Ann Surg 2003; 238:651.
18. Blumstein GW, Andras LM, Seehausen DA, et al. Fever is common postoperatively
following posterior spinal fusion: infection is an uncommon cause. J Pediatr 2015;
166:751.
19. Sharp NE, Alemayehu H, Desai A, et al. Fever after redo Nissen fundoplication with hiatal
hernia repair. J Surg Res 2014; 190:594.
20. Sazbon L, Groswasser Z. Outcome in 134 patients with prolonged posttraumatic
unawareness. Part 1: Parameters determining late recovery of consciousness. J
Neurosurg 1990; 72:75.
21. Horan TC, Culver DH, Gaynes RP, et al. Nosocomial infections in surgical patients in the
United States, January 1986-June 1992. National Nosocomial Infections Surveillance
(NNIS) System. Infect Control Hosp Epidemiol 1993; 14:73.
22. Manning BJ, Winter DC, McGreal G, et al. Nasogastric intubation causes
gastroesophageal reflux in patients undergoing elective laparotomy. Surgery 2001;
130:788.
23. Garibaldi RA, Burke JP, Dickman ML, Smith CB. Factors predisposing to bacteriuria during
indwelling urethral catheterization. N Engl J Med 1974; 291:215.
24. Sedor J, Mulholland SG. Hospital-acquired urinary tract infections associated with the
indwelling catheter. Urol Clin North Am 1999; 26:821.
25. Friedman C, Sturm LK, Chenoweth C. Electronic chart review as an aid to postdischarge
surgical site surveillance: increased case finding. Am J Infect Control 2001; 29:329.
26. Sands K, Vineyard G, Platt R. Surgical site infections occurring after hospital discharge. J
Infect Dis 1996; 173:963.
27. Ridderstolpe L, Gill H, Granfeldt H, et al. Superficial and deep sternal wound
complications: incidence, risk factors and mortality. Eur J Cardiothorac Surg 2001;
20:1168.
28. Delgado-Rodríguez M, Gómez-Ortega A, Sillero-Arenas M, Llorca J. Epidemiology of
surgical-site infections diagnosed after hospital discharge: a prospective cohort study.
Infect Control Hosp Epidemiol 2001; 22:24.
29. O'Grady NP, Barie PS, Bartlett JG, et al. Practice guidelines for evaluating new fever in
critically ill adult patients. Task Force of the Society of Critical Care Medicine and the
Infectious Diseases Society of America. Clin Infect Dis 1998; 26:1042.
30. Chadee DD, Tilluckdharry CC, Maharaj P, Sinanan C. Reactivation of Plasmodium
malariae infection in a Trinidadian man after neurosurgery. N Engl J Med 2000; 342:1924.
31. Mungai M, Tegtmeier G, Chamberland M, Parise M. Transfusion-transmitted malaria in the
United States from 1963 through 1999. N Engl J Med 2001; 344:1973.
32. Dodd RY. Transmission of parasites by blood transfusion. Vox Sang 1998; 74 Suppl
2:161.
33. McQuiston JH, Childs JE, Chamberland ME, Tabor E. Transmission of tick-borne agents
of disease by blood transfusion: a review of known and potential risks in the United States.
Transfusion 2000; 40:274.
34. Baddour LM, Bisno AL. Recurrent cellulitis after saphenous venectomy for coronary
bypass surgery. Ann Intern Med 1982; 97:493.
35. Baddour LM. Breast cellulitis complicating breast conservation therapy. J Intern Med 1999;
245:5.
36. Octavio J, Rosenberg W, Conte JE Jr. Surgical-wound infection with Pasteurella multocida
from pet dogs. N Engl J Med 2001; 345:549.
37.

http://www.fda.gov/downloads/BiologicsBloodVaccines/SafetyAvailability/ReportaProblem/
TransfusionDonationFatalities/UCM459461.pdf (Accessed on September 23, 2016).
38. Tan FL, Loo WL, Tan SG, et al. Severe acute respiratory syndrome in surgical patients: a
diagnostic dilemma. ANZ J Surg 2005; 75:21.
39. Papazian L, Fraisse A, Garbe L, et al. Cytomegalovirus. An unexpected cause of
ventilator-associated pneumonia. Anesthesiology 1996; 84:280.
40. Camazine B, Antkowiak JG, Nava ME, et al. Herpes simplex viral pneumonia in the
postthoracotomy patient. Chest 1995; 108:876.
41. Avery RK, Longworth DL. Viral pulmonary infections in thoracic and cardiovascular
surgery. Semin Thorac Cardiovasc Surg 1995; 7:88.
42. Wallace WC, Cinat ME, Nastanski F, et al. New epidemiology for postoperative
nosocomial infections. Am Surg 2000; 66:874.
43. Caplan ES, Hoyt NJ. Nosocomial sinusitis. JAMA 1982; 247:639.
44. Borman KR, Brown PM, Mezera KK, Jhaveri H. Occult fever in surgical intensive care unit
patients is seldom caused by sinusitis. Am J Surg 1992; 164:412.
45. Raad II, Sabbagh MF, Caranasos GJ. Acute bacterial sialadenitis: a study of 29 cases and
review. Rev Infect Dis 1990; 12:591.
46. Huffman JL, Schenker S. Acute acalculous cholecystitis: a review. Clin Gastroenterol
Hepatol 2010; 8:15.
47. Morrison VA, Oldfield EC 3rd. Postoperative toxic shock syndrome. Arch Surg 1983;
118:791.
48. Odom SR, Stallard JD, Pacheco HO, Ho H. Postoperative staphylococcal toxic shock
syndrome due to pre-existing staphylococcal infection: case report and review of the
literature. Am Surg 2001; 67:745.
49. Cobb WS, Paton BL, Novitsky YW, et al. Intra-abdominal placement of antimicrobial-
impregnated mesh is associated with noninfectious fever. Am Surg 2006; 72:1205.
50. Suzuki K, Sieczka E, Tranbaugh R, Hoffman D. Pyoderma gangrenosum after cardiac
surgery masquerading as a fulminant sternal wound infection. Int J Surg Case Rep 2015;
6C:163.
51. Aday AW, Saavedra AP, Levy BD, Loscalzo J. CLINICAL PROBLEM-SOLVING.
Prevention as Precipitant. N Engl J Med 2016; 375:471.
52. Craig MH, Poole GV, Hauser CJ. Postsurgical gout. Am Surg 1995; 61:56.
53. Masuda I, Ishikawa K. Clinical features of pseudogout attack. A survey of 50 cases. Clin
Orthop Relat Res 1988; :173.
54. Hughes SG, Chekan EG, Ali A, et al. Unusual complications following laparoscopic Nissen
fundoplication. Surg Laparosc Endosc Percutan Tech 1999; 9:143.
55. Pape HC, Giannoudis P, Krettek C. The timing of fracture treatment in polytrauma
patients: relevance of damage control orthopedic surgery. Am J Surg 2002; 183:622.
56. Pell AC, Christie J, Keating JF, Sutherland GR. The detection of fat embolism by
transoesophageal echocardiography during reamed intramedullary nailing. A study of 24
patients with femoral and tibial fractures. J Bone Joint Surg Br 1993; 75:921.
57. Pitto RP, Hamer H, Fabiani R, et al. Prophylaxis against fat and bone-marrow embolism
during total hip arthroplasty reduces the incidence of postoperative deep-vein thrombosis:
a controlled, randomized clinical trial. J Bone Joint Surg Am 2002; 84-A:39.
58. Jenkins K, Chung F, Wennberg R, et al. Fat embolism syndrome and elective knee
arthroplasty. Can J Anaesth 2002; 49:19.
59. Platt MS, Kohler LJ, Ruiz R, et al. Deaths associated with liposuction: case reports and
review of the literature. J Forensic Sci 2002; 47:205.
60. Vichinsky EP, Neumayr LD, Earles AN, et al. Causes and outcomes of the acute chest
syndrome in sickle cell disease. National Acute Chest Syndrome Study Group. N Engl J
Med 2000; 342:1855.
61. Prince SE, Cunha BA. Postpericardiotomy syndrome. Heart Lung 1997; 26:165.
62. Koennecke HC, Leistner S. Prophylactic antipyretic treatment with acetaminophen in acute
ischemic stroke: a pilot study. Neurology 2001; 57:2301.
63. Oliveira-Filho J, Ezzeddine MA, Segal AZ, et al. Fever in subarachnoid hemorrhage:
relationship to vasospasm and outcome. Neurology 2001; 56:1299.
64. Ness PM, Shirey RS, Weinstein MH, King KE. An animal model for delayed hemolytic
transfusion reactions. Transfus Med Rev 2001; 15:305.
65. Kopko PM, Marshall CS, MacKenzie MR, et al. Transfusion-related acute lung injury:
report of a clinical look-back investigation. JAMA 2002; 287:1968.
66. So PC. Unmasking of thyrotoxicosis during anaesthesia. Hong Kong Med J 2001; 7:311.
67. Lee KS, Kim K, Hur KB, Kim CK. The role of propranolol in the preoperative preparation of
patients with Graves' disease. Surg Gynecol Obstet 1986; 162:365.
68. Lynch BA, Dolan JP, Mann M. Thyrotoxicosis after gastric bypass surgery prompting
operative re-exploration. Obes Surg 2005; 15:883.
69. Siu SC, Kitzman DW, Sheedy PF 2nd, Northcutt RC. Adrenal insufficiency from bilateral
adrenal hemorrhage. Mayo Clin Proc 1990; 65:664.
70. Rao RH, Vagnucci AH, Amico JA. Bilateral massive adrenal hemorrhage: early recognition
and treatment. Ann Intern Med 1989; 110:227.
71. Vella A, Nippoldt TB, Morris JC 3rd. Adrenal hemorrhage: a 25-year experience at the
Mayo Clinic. Mayo Clin Proc 2001; 76:161.
72. Udelsman R, Ramp J, Gallucci WT, et al. Adaptation during surgical stress. A reevaluation
of the role of glucocorticoids. J Clin Invest 1986; 77:1377.
73. Roberts J, Barnes W, Pennock M, Browne G. Diagnostic accuracy of fever as a measure
of postoperative pulmonary complications. Heart Lung 1988; 17:166.
74. Engoren M. Lack of association between atelectasis and fever. Chest 1995; 107:81.
75. Brown FE, Nierenberg DW, Nordgren RE, et al. Neuroleptic malignant syndrome:
occurrence in a child after reconstructive surgery. Plast Reconstr Surg 1991; 87:961.
76. Pien F, Ho PW, Fergusson DJ. Fever and infection after cardiac operation. Ann Thorac
Surg 1982; 33:382.
77. Wilson AP, Treasure T, Grüneberg RN, et al. Should the temperature chart influence
management in cardiac operations? Result of a prospective study in 314 patients. J
Thorac Cardiovasc Surg 1988; 96:518.
78. Kreuzer E, Kääb S, Pilz G, Werdan K. Early prediction of septic complications after cardiac
surgery by APACHE II score. Eur J Cardiothorac Surg 1992; 6:524.
79. Leal-Noval SR, Rincón-Ferrari MD, García-Curiel A, et al. Transfusion of blood
components and postoperative infection in patients undergoing cardiac surgery. Chest
2001; 119:1461.
80. Perrault LP, Kirkwood KA, Chang HL, et al. A Prospective Multi-Institutional Cohort Study
of Mediastinal Infections After Cardiac Operations. Ann Thorac Surg 2018; 105:461.
81. Bor DH, Rose RM, Modlin JF, et al. Mediastinitis after cardiovascular surgery. Rev Infect
Dis 1983; 5:885.
82. Fariñas MC, Gald Peralta F, Bernal JM, et al. Suppurative mediastinitis after open-heart
surgery: a case-control study covering a seven-year period in Santander, Spain. Clin Infect
Dis 1995; 20:272.
83. El Oakley RM, Wright JE. Postoperative mediastinitis: classification and management. Ann
Thorac Surg 1996; 61:1030.
84. Milano CA, Kesler K, Archibald N, et al. Mediastinitis after coronary artery bypass graft
surgery. Risk factors and long-term survival. Circulation 1995; 92:2245.
85. Trouillet JL, Vuagnat A, Combes A, et al. Acute poststernotomy mediastinitis managed
with debridement and closed-drainage aspiration: factors associated with death in the
intensive care unit. J Thorac Cardiovasc Surg 2005; 129:518.
86. Risnes I, Abdelnoor M, Almdahl SM, Svennevig JL. Mediastinitis after coronary artery
bypass grafting risk factors and long-term survival. Ann Thorac Surg 2010; 89:1502.
87. Kohman LJ, Coleman MJ, Parker FB Jr. Bacteremia and sternal infection after coronary
artery bypass grafting. Ann Thorac Surg 1990; 49:454.
88. Mossad SB, Serkey JM, Longworth DL, et al. Coagulase-negative staphylococcal sternal
wound infections after open heart operations. Ann Thorac Surg 1997; 63:395.
89. Muñoz P, Menasalvas A, Bernaldo de Quirós JC, et al. Postsurgical mediastinitis: a case-
control study. Clin Infect Dis 1997; 25:1060.
90. Liu JY, Birkmeyer NJ, Sanders JH, et al. Risks of morbidity and mortality in dialysis
patients undergoing coronary artery bypass surgery. Northern New England
Cardiovascular Disease Study Group. Circulation 2000; 102:2973.
91. Gummert JF, Barten MJ, Hans C, et al. Mediastinitis and cardiac surgery--an updated risk
factor analysis in 10,373 consecutive adult patients. Thorac Cardiovasc Surg 2002; 50:87.
92. Gottlieb GS, Fowler VG Jr, Kong LK, et al. Staphylococcus aureus bacteremia in the
surgical patient: a prospective analysis of 73 postoperative patients who developed
Staphylococcus aureus bacteremia at a tertiary care facility. J Am Coll Surg 2000; 190:50.
93. Fowler VG Jr, Kaye KS, Simel DL, et al. Staphylococcus aureus bacteremia after median
sternotomy: clinical utility of blood culture results in the identification of postoperative
mediastinitis. Circulation 2003; 108:73.
94. Tammelin A, Hambraeus A, Ståhle E. Mediastinitis after cardiac surgery: improvement of
bacteriological diagnosis by use of multiple tissue samples and strain typing. J Clin
Microbiol 2002; 40:2936.
95. Weber SF, Washburn RG. Invasive Aspergillus infections complicating coronary artery
bypass grafting. South Med J 1990; 83:584.
96. Isenberg HD, Tucci V, Cintron F, et al. Single-source outbreak of Candida tropicalis
complicating coronary bypass surgery. J Clin Microbiol 1989; 27:2426.
97. Webber SA, Wilson NJ, Junker AK, et al. Postpericardiotomy syndrome: no evidence for a
viral etiology. Cardiol Young 2001; 11:67.
98. Kaufman BA, Tunkel AR, Pryor JC, Dacey RG Jr. Meningitis in the neurosurgical patient.
Infect Dis Clin North Am 1990; 4:677.
99. Forgacs P, Geyer CA, Freidberg SR. Characterization of chemical meningitis after
neurological surgery. Clin Infect Dis 2001; 32:179.
100. Zhang Y, Xiao X, Zhang J, et al. Diagnostic accuracy of routine blood examinations
and CSF lactate level for post-neurosurgical bacterial meningitis. Int J Infect Dis 2017;
59:50.
101. Hernández Ortiz OH, García García HI, Muñoz Ramírez F, et al. Development of a
prediction rule for diagnosing postoperative meningitis: a cross-sectional study. J
Neurosurg 2018; 128:262.
102. Chatzisotiriou AS, Selviaridis PK, Kontopoulos VA, et al. Delayed persistent
hyperthermia after resection of a craniopharyngioma. Pediatr Neurosurg 2004; 40:196.
103. Blum U, Voshage G, Lammer J, et al. Endoluminal stent-grafts for infrarenal
abdominal aortic aneurysms. N Engl J Med 1997; 336:13.
104. Velázquez OC, Carpenter JP, Baum RA, et al. Perigraft air, fever, and leukocytosis
after endovascular repair of abdominal aortic aneurysms. Am J Surg 1999; 178:185.
105. Storck M, Scharrer-Pamler R, Kapfer X, et al. Does a postimplantation syndrome
following endovascular treatment of aortic aneurysms exist? Vasc Surg 2001; 35:23.
106. Bölke E, Jehle PM, Storck M, et al. Endovascular stent-graft placement versus
conventional open surgery in infrarenal aortic aneurysm: a prospective study on acute
phase response and clinical outcome. Clin Chim Acta 2001; 314:203.
107. Romano F, Caprotti R, Conti M, et al. Thrombosis of the splenoportal axis after
splenectomy. Langenbecks Arch Surg 2006; 391:483.
108. Schwandt A, Andrews SJ, Fanning J. Prospective analysis of a fever evaluation
algorithm after major gynecologic surgery. Am J Obstet Gynecol 2001; 184:1066.
109. Schey D, Salom EM, Papadia A, Penalver M. Extensive fever workup produces low
yield in determining infectious etiology. Am J Obstet Gynecol 2005; 192:1729.
110. Tanabe K, Takahashi K, Tokumoto T, et al. Infectious complications in ABO-
incompatible living donor kidney transplantation: a single center experience. Transplant
Proc 1998; 30:3130.
111. Fishman JA, Rubin RH. Infection in organ-transplant recipients. N Engl J Med
1998; 338:1741.
112. Yoshikawa T, Ihira M, Furukawa H, et al. Four cases of human herpesvirus 6
variant B infection after pediatric liver transplantation. Transplantation 1998; 65:1266.
113. Badillo AT, Sarani B, Evans SR. Optimizing the use of blood cultures in the febrile
postoperative patient. J Am Coll Surg 2002; 194:477.
114. Takakura Y, Hinoi T, Egi H, et al. Procalcitonin as a predictive marker for surgical
site infection in elective colorectal cancer surgery. Langenbecks Arch Surg 2013; 398:833.
115. Clec'h C, Fosse JP, Karoubi P, et al. Differential diagnostic value of procalcitonin in
surgical and medical patients with septic shock. Crit Care Med 2006; 34:102.
116. Meisner M, Tschaikowsky K, Hutzler A, et al. Postoperative plasma concentrations
of procalcitonin after different types of surgery. Intensive Care Med 1998; 24:680.
117. Michalik DE, Duncan BW, Mee RB, et al. Quantitative analysis of procalcitonin after
pediatric cardiothoracic surgery. Cardiol Young 2006; 16:48.
118. Plaisance KI, Mackowiak PA. Antipyretic therapy: physiologic rationale, diagnostic
implications, and clinical consequences. Arch Intern Med 2000; 160:449.