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Postoperative fever

Postoperative fever is an elevated body temperature that develops in the period following a surgical procedure, commonly defined as a temperature exceeding 38°C (100.4°F) on two consecutive postoperative days or greater than 39°C (102.2°F) on any single postoperative day.^[1] This condition is prevalent among surgical patients, with reported incidence rates ranging from 20% to 90%, influenced by factors such as the type of surgery, patient comorbidities, and operative duration; it is particularly common after abdominal, thoracic, and orthopedic procedures.^[1] While often transient and related to the normal inflammatory response to tissue trauma, postoperative fever can signal serious underlying issues, necessitating prompt evaluation to differentiate benign etiologies from life-threatening infections.^[1] The etiology of postoperative fever encompasses both infectious and noninfectious causes, with the timing of onset providing key diagnostic clues.^[1] A widely used mnemonic, the "5 Ws," aids in recalling common sources: Wind (pulmonary complications such as atelectasis on postoperative days [POD] 1–2 or pneumonia on POD 3), Water (urinary tract infections on POD 3–5, often linked to catheterization), Wound (surgical site infections or abscesses on POD 4–7), Walking (deep vein thrombosis or thrombophlebitis on POD 3–7), and Wonder drugs (drug-induced fever or central line infections beyond POD 7).^[2] Noninfectious contributors, including transfusion reactions, malignant hyperthermia, or pancreatitis, may also manifest early, while delayed fevers heighten suspicion for endovascular infections or anastomotic leaks.^[1] Evaluation of postoperative fever involves a systematic approach starting with a detailed history of the surgery, medications, and symptoms, followed by physical examination focusing on vital signs, surgical sites, lungs, and extremities.^[1] Laboratory investigations typically include complete blood count, blood and urine cultures, C-reactive protein, and procalcitonin levels to assess for inflammation or infection, with imaging such as chest X-ray, ultrasound, or computed tomography guided by suspected sources.^[2] Management prioritizes source control, such as removing unnecessary catheters or draining abscesses, alongside supportive care with intravenous fluids, oxygen, and antipyretics; empiric antibiotics are reserved for cases with evidence of infection to avoid resistance, and multidisciplinary input from infectious disease specialists may be required for complex scenarios.^[1] Timely intervention is essential, as untreated infectious causes can progress to sepsis, increasing morbidity and mortality.^[1]

Definition and Epidemiology

Definition

Postoperative fever is defined as a temperature higher than 38°C (100.4°F) on two consecutive postoperative days or higher than 39°C (102.2°F) on any postoperative day.^[1] This elevation should be measured via core routes such as rectal, esophageal, or pulmonary artery methods to distinguish it from peripheral temperature increases, which may not reflect true hyperthermia.^[3] The condition is common following surgical procedures due to the body's response to tissue trauma, but it requires careful evaluation to identify underlying issues. A key distinction exists between physiologic and pathologic postoperative fever. Physiologic fever represents a benign, self-limited response to surgical stress, often resolving without intervention.^[4] In contrast, pathologic fever is indicative of an underlying disorder, marked by prolonged duration and accompanying signs such as tachycardia, leukocytosis, or organ dysfunction.^[4] Postoperative fever is classified temporally to guide differential diagnosis using common frameworks such as immediate (postoperative day [POD] 0–1), acute (POD 1–7), subacute (1–4 weeks), and delayed (>4 weeks).^[1] Early fevers are often noninfectious, while later ones increase suspicion for infections or complications. This entity excludes intraoperative temperature elevations, which may stem from anesthetic agents or procedural factors, as well as immediate postanesthesia shivering, a thermoregulatory response to hypothermia rather than true pyrexia.^[1]

Incidence and Risk Factors

Postoperative fever is a common occurrence following surgery, with reported incidence rates ranging from 14% to 91% across various procedures, depending on the definition of fever and the type of surgery performed.^[5] In general surgical populations, rates typically fall between 20% and 50%, while early postoperative fever (within the first 48 hours) can affect up to 50-70% of patients due to inflammatory responses.^[1]^[6] Higher incidences are observed in major abdominal or thoracic surgeries, reaching up to 50%, whereas minor procedures exhibit lower rates, often below 20%.^[7] For elective surgeries, a 2025 study on minimally invasive resections for gastric and colorectal cancer reported an incidence of 12.6%, highlighting variability even within elective contexts.^[7] Patient-related risk factors significantly influence the likelihood of developing postoperative fever. Advanced age over 60 years increases susceptibility due to diminished physiological reserves and comorbidities.^[5] Obesity, defined by a body mass index greater than 30 kg/m², is associated with higher rates through mechanisms like impaired wound healing and increased inflammation.^[5] Diabetes mellitus elevates risk by compromising immune function and glycemic control, while immunosuppression from conditions such as chemotherapy or organ transplantation further heightens vulnerability.^[1] Smoking history is a notable contributor, as it impairs pulmonary function and promotes infection.^[5] Surgery-related factors also play a critical role in postoperative fever incidence. Emergency procedures carry elevated risks compared to elective ones, owing to less optimal preoperative preparation and higher contamination potential.^[5] Operative duration exceeding 2 hours is independently associated with increased fever, as longer exposure correlates with greater tissue trauma and bacterial load.^[1] Contaminated or dirty wounds, classified per surgical wound categories, substantially raise the odds of febrile complications.^[1] Procedure-specific differences are evident, with colorectal surgeries showing higher rates (up to 40%) than orthopedic procedures (around 10-20%), reflecting variations in anatomical involvement and microbial exposure.^[7]^[8] Demographic trends indicate that females may experience higher rates of postoperative fever linked to certain infections, such as urinary tract infections following pelvic surgery.^[9] Globally, variations exist due to healthcare access, with low-resource settings reporting higher surgical site infection rates—a common cause of fever—up to 23% for gastrointestinal surgeries, compared to 1-5% in high-income countries, attributable to limited sterilization and antibiotic availability.^[10]

Causes

Noninfectious Causes

Noninfectious causes account for the majority of postoperative fevers, often arising from the body's inflammatory response to surgical trauma, medications, or procedural complications, and typically resolve without specific intervention.^[1] These etiologies are particularly prevalent in the early postoperative period and must be distinguished from infectious processes to avoid unnecessary antimicrobial therapy. A common mnemonic for recalling potential causes of postoperative fever is the "5 Ws": Wind (atelectasis), Water (urinary tract issues, though often infectious), Wound (surgical site, often infectious), Walking (thrombotic events), and Wonder drugs (medication reactions), with noninfectious elements emphasizing atelectasis, thrombosis, and drug effects.^[11] Atelectasis, or partial lung collapse, is one of the most frequent noninfectious causes, occurring in up to 90% of postoperative patients undergoing general anesthesia due to shallow breathing from pain, anesthesia, or immobility, typically within the first 1 to 3 days after surgery.^[12] While atelectasis is common in the early postoperative period and has been traditionally associated with fever, evidence does not support a causal relationship.^[13] It often presents with mild respiratory symptoms such as dyspnea or reduced breath sounds and is usually benign and self-limited, resolving with deep breathing exercises or incentive spirometry.^[3] Deep vein thrombosis (DVT) and pulmonary embolism (PE) represent thrombotic noninfectious causes, emerging around postoperative days 3 to 7 due to venous stasis from immobility and surgical stress, with DVT often affecting the lower extremities and PE involving embolization to the lungs.^[1] Symptoms may include unilateral leg swelling, pain, or calf tenderness for DVT, and acute dyspnea, tachycardia, or pleuritic chest pain for PE, though fever is typically low-grade and resolves with anticoagulation therapy such as heparin.^[3] These events underscore the importance of early mobilization in surgical recovery to mitigate risk. Drug fever arises as an idiosyncratic hypersensitivity reaction to perioperative medications, including antibiotics, anesthetics, or analgesics, usually manifesting subacutely around postoperative day 5 to 10 and diagnosed by exclusion after other causes are ruled out.^[1] It is characterized by fever often accompanied by rash, arthralgias, or peripheral eosinophilia, and cessation of the offending agent leads to prompt resolution, highlighting the need for careful medication review in febrile patients.^[3] Transfusion reactions, particularly febrile non-hemolytic types, occur immediately after administration of blood products, within 1 to 6 hours postoperatively, triggered by recipient antibodies against donor leukocytes or cytokines in stored blood.^[1] These present with chills, rigors, and fever without evidence of hemolysis, and management involves halting the transfusion and providing antipyretics, with premedication strategies like acetaminophen used prophylactically in at-risk patients.^[3] Other noninfectious causes include procedure-specific complications such as pancreatitis following abdominal surgery, which can cause fever through inflammatory enzyme release and abdominal pain around postoperative days 2 to 7, and thyroiditis after neck procedures like thyroidectomy, leading to fever from glandular inflammation and potential transient thyrotoxicosis.^[3] These rarer etiologies emphasize the role of surgical site in fever generation, with overall noninfectious processes comprising up to 90% of early postoperative fevers in some cohorts.^[1]

Infectious Causes

Infectious causes of postoperative fever arise from microbial invasion at surgical or procedural sites, with bacterial pathogens predominating and incidence increasing over time as the risk of contamination and device-related colonization rises. These etiologies account for 20-30% of postoperative fevers overall, though early-onset infections (within 48 hours) remain rare unless preoperative contamination or bacteremia is present. Common pathogens include gram-positive cocci like Staphylococcus aureus and gram-negative rods like Escherichia coli, varying by site.^[1]^[14]^[15] Surgical site infections (SSIs), encompassing superficial and deep wound infections, typically manifest between postoperative days 5 and 10, with local signs such as erythema, warmth, tenderness, and purulent drainage indicating involvement. These infections often stem from skin flora like Staphylococcus aureus or Streptococcus species, particularly in contaminated procedures or those exceeding 2 hours in duration.^[1]^[14] Urinary tract infections (UTIs) frequently emerge around days 3 to 5, especially in patients with indwelling Foley catheters that facilitate bacterial ascension. Clinical features include dysuria, urinary frequency, and suprapubic discomfort, with diagnosis relying on urine cultures showing greater than 10^5 colony-forming units per milliliter of pathogens such as Escherichia coli or Enterococcus species.^[1]^[14] Respiratory infections, such as pneumonia or ventilator-associated events, may occur early in intubated patients but more commonly develop by days 3 to 5, presenting with cough, dyspnea, tachypnea, and radiographic infiltrates on chest X-ray. Causative organisms often include Streptococcus pneumoniae, Haemophilus influenzae, or aspiration-related anaerobes, heightened in prolonged mechanical ventilation scenarios.^[1]^[14] Intra-abdominal abscesses represent late-onset infections, peaking beyond day 7 (often 1-4 weeks postoperatively), particularly following gastrointestinal surgery, and feature localized abdominal pain, distension, and leukocytosis. These collections arise from polymicrobial flora, including anaerobes and Enterobacteriaceae, requiring imaging for confirmation.^[1]^[14] Additional sources encompass intravascular catheter-related bacteremia, which can cause immediate high-grade fever (>40°C) with chills due to Staphylococcus species from central lines, and Clostridium difficile colitis triggered by perioperative antibiotics, manifesting as profuse diarrhea typically 3-10 days post-exposure. Diabetes and immunosuppression elevate risk across these infectious etiologies.^[1]^[14]

Pathophysiology

Surgical Inflammatory Response

Surgical trauma initiates a systemic inflammatory response characterized by the release of proinflammatory cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) from damaged tissues and activated immune cells, including macrophages and endothelial cells.^[16]^[17] These cytokines act on the hypothalamus to induce the synthesis of prostaglandin E2 (PGE2), which elevates the body's thermoregulatory set point, resulting in fever as a component of this adaptive response.^[17]^[16] This inflammatory cascade often manifests as an adaptation of the systemic inflammatory response syndrome (SIRS) criteria, where fever (>38°C or <36°C) combines with other signs such as tachycardia (heart rate >90 beats per minute) and leukocytosis (white blood cell count >12,000/μL or <4,000/μL) in the absence of infection.^[1]^[18] Unlike full SIRS triggered by severe insults, the postoperative variant is typically self-limited and reflects the body's attempt to repair tissue damage without progressing to widespread immune dysregulation.^[18] The intensity of this response is amplified by surgical factors, including the extent of tissue manipulation, which releases damage-associated molecular patterns (DAMPs) that further stimulate cytokine production; significant blood loss, which activates complement and coagulation pathways; and the insertion of foreign bodies like drains, promoting localized inflammation that contributes to systemic effects.^[16]^[18] More invasive procedures, such as those involving prolonged operative times or extensive dissection, correlate with higher cytokine levels and greater fever magnitude.^[17] In uncomplicated cases, the inflammatory response peaks within 24 to 48 hours postoperatively, driven by maximal IL-6 and PGE2 activity, and typically resolves by postoperative day 3 as cytokine levels decline and anti-inflammatory mechanisms, such as IL-6-mediated production of antagonists, predominate.^[17]^[16] This pattern accounts for the majority of early postoperative fevers, which are benign and noninfectious in origin.^[1] Distinguishing this response from sepsis is critical, as the surgical inflammatory state lacks evidence of organ dysfunction—such as altered mental status, hypotension requiring vasopressors, or acute kidney injury—required for septic diagnoses.^[1] Monitoring trends in C-reactive protein (CRP), an acute-phase reactant induced by IL-6 that peaks at 48 to 72 hours and declines thereafter in the absence of complications, helps confirm resolution and rule out escalating infection.^[19]^[18] Persistent CRP elevation beyond day 3 or a failure to trend downward warrants further evaluation.^[19]

Mechanism of Fever Generation

Fever generation in the postoperative period involves a pyrogen cascade initiated by inflammatory signals from surgical trauma. Exogenous pyrogens, such as bacterial endotoxins like lipopolysaccharide from potential contaminants, or endogenous pyrogens including cytokines (e.g., IL-1, IL-6, TNF-α), are released by activated immune cells such as macrophages. These pyrogens cross or signal through the blood-brain barrier to reach the hypothalamus, where they induce the expression of cyclooxygenase-2 (COX-2) in endothelial cells of the preoptic area. COX-2 catalyzes the production of prostaglandin E2 (PGE2), which binds to EP3 receptors on hypothalamic neurons, elevating the thermoregulatory set point by approximately 1-2°C above baseline (typically from 37°C to 38-39°C). This reset in the anterior hypothalamus triggers physiological responses like vasoconstriction and shivering to conserve and generate heat, maintaining the elevated temperature until the pyrogenic stimulus resolves.^[20]^[21]^[22]^[23] Interactions between endothelial cells and immune components further amplify this process postoperatively. Neutrophil activation occurs rapidly in response to tissue injury, promoting the acute phase response via cytokine signaling that stimulates hepatic production of proteins such as ferritin (which sequesters iron to limit microbial growth) and fibrinogen (which supports clot formation and endothelial repair). These acute phase reactants rise within hours of surgery, contributing to systemic inflammation that sustains pyrogen release and fever. In the postoperative setting, this response is particularly pronounced due to the sterile inflammatory milieu created by surgical manipulation.^[24] Specific postoperative factors can independently trigger or exacerbate the pyrogen cascade. Reversal of intraoperative hypothermia—common under general anesthesia due to impaired thermoregulation and heat loss—often leads to a rebound elevation in core temperature as vasoconstriction activates and metabolic rate increases to restore homeostasis. Additionally, resorption of hematomas or seromas releases cellular debris and pyrogenic cytokines locally, inducing inflammation and fever without infection; for instance, hematoma breakdown can elevate IL-6 levels, perpetuating the COX-2/PGE2 pathway.^[25]^[26] Regulatory feedback loops modulate fever duration to prevent excessive hyperthermia. Interleukin-10 (IL-10), an anti-inflammatory cytokine produced by immune cells, acts as an endogenous antipyretic by inhibiting pro-inflammatory cytokines like IL-6 and TNF-α, thereby reducing PGE2 synthesis and promoting defervescence. Endogenous IL-10 limits fever amplitude and duration in models of inflammation; for instance, its neutralization increases peak temperature by 0.4–0.6°C and prolongs fever duration (e.g., >72 hours for LPS-induced fever vs. ~10 hours in controls). Its deficiency sustains the inflammatory cascade by failing to adequately counter pro-inflammatory signals.^[27]

Clinical Presentation

Symptoms and Signs

Postoperative fever primarily manifests as an elevated body temperature exceeding 38°C (100.4°F) on two consecutive days or 39°C (102.2°F) on any postoperative day, often accompanied by core symptoms such as chills, rigors, and diaphoresis.^[1] These symptoms arise from the body's thermoregulatory response, where rigors represent involuntary muscle contractions to generate heat, and diaphoresis follows as the temperature set point normalizes.^[22] Fever spikes in postoperative patients frequently exhibit a diurnal pattern, peaking in the late afternoon or evening due to circadian influences on cytokine release and hypothalamic activity.^[28] Site-specific signs provide clues to the underlying etiology and guide clinical suspicion. For surgical site infections (SSIs), patients may present with localized wound tenderness, erythema, warmth, and purulent discharge.^[1] In cases of pyelonephritis, flank pain and costovertebral angle tenderness are common, while deep vein thrombosis (DVT) often involves unilateral calf tenderness, swelling, and warmth.^[3] These localized findings, when combined with fever, heighten concern for infectious or thrombotic complications at the affected site.^[14] Systemic manifestations extend beyond the fever itself and include malaise, anorexia, and alterations in vital signs. Tachycardia exceeding 100 beats per minute is frequent, reflecting the sympathetic response to pyrogens, while severe cases may involve hypotension indicative of sepsis or hypovolemia.^[1] These symptoms contribute to the systemic inflammatory response syndrome (SIRS) criteria, which encompass temperature extremes, heart rate elevation, and tachypnea.^[1] Atypical presentations are particularly relevant in vulnerable populations. Elderly patients may exhibit blunted fever responses, with altered mental status, confusion, or lethargy occurring without pronounced temperature elevation, as immunosenescence impairs the febrile reaction.^[29] Similarly, immunocompromised individuals, such as those on chemotherapy or post-transplant, often display minimal or absent fever alongside subtle signs like worsening fatigue, due to suppressed inflammatory pathways.^[3] Regarding duration, a single isolated fever spike is often self-limited and physiologic, particularly in the early postoperative period, but sustained fever persisting beyond three days raises suspicion for an underlying pathology requiring evaluation.^[1] Prolonged elevation disrupts homeostasis and correlates with increased morbidity if untreated.^[14]

Temporal Patterns

Postoperative fever manifests in distinct temporal patterns based on its onset relative to surgery, which aids in narrowing differential diagnoses for etiology. Early postoperative fever, occurring on postoperative days (POD) 0 to 2, affects 15% to 90% of surgical patients and is predominantly noninfectious, with studies indicating that up to 92% of cases in this period stem from surgical inflammation or atelectasis. These fevers are characteristically transient, often resolving spontaneously within 72 hours, and typically mild with temperatures below 38.5°C, peaking around POD 1.^[30]^[1] In the intermediate period (POD 3 to 5), fevers such as those linked to urinary tract infections or deep vein thrombosis/pulmonary embolism become more prominent and may persist without intervention, contrasting with the self-limiting nature of early fevers.^[1] Late postoperative fever, arising after POD 5, signals a higher likelihood of serious complications including surgical site infections or abscesses, with approximately 90% of such cases involving identifiable infections; these episodes often feature high-grade temperatures exceeding 39°C and a remittent pattern of spikes and partial resolutions.^[30] Fever patterns vary between continuous elevation, common in untreated infectious processes, and intermittent spikes, more typical of resolving inflammatory responses, with defervescence generally aligning with effective treatment of the underlying cause. Prognostically, fever persisting beyond 5 days elevates the odds of infection (with odds ratios exceeding 20 in some analyses for delayed onset), while bimodal patterns—fevers recurring after initial resolution—often indicate multifactorial contributors.^[30]^[1]

Diagnostic Approach

History and Physical Examination

The evaluation of postoperative fever commences with a detailed history and physical examination, which serve as the cornerstone for identifying potential causes and directing subsequent investigations without relying on invasive or laboratory-based assessments. A thorough history helps contextualize the fever within the surgical context and uncovers site-specific clues that inform the differential diagnosis. Key historical elements include the specifics of the surgical procedure, such as its type (e.g., abdominal, orthopedic), duration, degree of contamination (clean, contaminated, or dirty), and any intraoperative complications like excessive blood loss or tissue trauma. The timing of fever onset—whether immediate (within hours) or delayed (after postoperative day 3)—is particularly informative, as early fevers are often noninfectious while later ones raise concern for infection. Inquire about the onset and pattern of associated symptoms via a targeted review of systems, including dysuria or frequency for urinary tract involvement, productive cough or dyspnea for respiratory sources, abdominal pain or distension for intra-abdominal processes, and unilateral leg pain or swelling for venous thromboembolism. Document relevant comorbidities (e.g., diabetes, immunosuppression), current medications including perioperative antibiotics or analgesics, recent procedures (e.g., central line placement), and exposures such as blood transfusions that could precipitate fever. The physical examination should be systematic and focused on common postoperative sites of pathology, beginning with vital signs to capture the fever curve (serial oral or rectal temperatures) alongside heart rate, blood pressure, respiratory rate, and oxygen saturation for evidence of systemic instability. Evaluate the patient's general appearance, mental status, and hydration; for instance, confusion or lethargy may signal central nervous system involvement or sepsis. Inspect the surgical wound and drains for local signs of infection, such as erythema, warmth, fluctuance, tenderness, or purulent drainage, while noting any surrounding cellulitis or dehiscence. Auscultate the lungs bilaterally for crackles, wheezes, or asymmetric breath sounds suggestive of atelectasis, pneumonia, or pleural effusion, and percuss for dullness. Palpate the lower extremities for calf tenderness, warmth, or edema indicating deep vein thrombosis, and examine intravenous access sites, oral mucosa, and the abdomen for tenderness, guarding, or rebound. Additional targeted checks include joint palpation for septic arthritis in relevant surgeries and skin survey for rashes or phlebitis. Red flags warranting urgent attention include hemodynamic instability (e.g., hypotension or tachycardia), oliguria, acute confusion, or respiratory distress, which collectively suggest sepsis, shock, or life-threatening complications like anastomotic leak or pulmonary embolism. Meticulous serial examinations on a regular basis, ideally every 4 to 6 hours in persistently febrile patients, facilitate ongoing monitoring and early recognition of evolving findings. A well-performed history and physical examination frequently identifies the source of fever among common etiologies, thereby optimizing resource use and avoiding unnecessary testing.

Laboratory and Imaging Studies

Laboratory and imaging studies play a crucial role in evaluating postoperative fever by providing objective data to support or refute suspected etiologies, particularly when guided by clinical history and examination findings. Initial laboratory evaluation often begins with a complete blood count (CBC), where leukocytosis exceeding 12,000/μL may suggest an infectious process, although it can also occur in noninfectious inflammation.^[1] C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are acute-phase reactants that are typically elevated in both inflammatory and infectious postoperative states; serial measurements of CRP, showing a rising trend, can help differentiate ongoing infection from expected surgical response.^[1]^[31] Urinalysis with microscopy and culture is recommended if urinary tract infection (UTI) is suspected, with pyuria typically defined as more than 5-10 white blood cells per high-power field (WBC/hpf) suggesting possible inflammation; for catheter-associated UTI common postoperatively, confirmation requires symptoms plus urine culture growth of at least 10^3 colony-forming units/mL.^[32] Blood cultures should be obtained if sepsis is suspected, particularly in hemodynamically unstable patients, but routine use is discouraged due to low yield and risk of contamination leading to unnecessary antibiotics.^[1] Similarly, microbiology studies such as wound swabs or sputum cultures are targeted based on site-specific symptoms; for example, sputum culture is useful in suspected pneumonia, while wound cultures guide management of surgical site infections without routine application to avoid overuse.^[1] Imaging studies are selected based on the suspected cause and timing of fever. Chest X-ray (CXR) is a first-line test for early postoperative fever to evaluate for atelectasis or pneumonia, with findings like infiltrates supporting infectious etiology.^[1] For thrombotic concerns, particularly around postoperative days 4-7, lower extremity venous ultrasound (US) is preferred to detect deep vein thrombosis (DVT), offering high sensitivity without radiation exposure.^[1] In cases of persistent fever suggesting intra-abdominal complications, computed tomography (CT) of the abdomen and pelvis identifies abscesses or collections with high accuracy, especially after day 7.^[1] Magnetic resonance imaging (MRI) is reserved for suspected spinal involvement, such as epidural abscess in neurosurgical patients, providing detailed soft tissue evaluation.^[1] Advanced biomarkers like procalcitonin (PCT) can aid in distinguishing bacterial infections from noninfectious inflammation, with levels above 0.5 ng/mL favoring bacterial etiology in postoperative settings, though cutoffs of 0.1-0.5 ng/mL are used for initial differentiation.^[33] Diagnostic tests overall have a low positivity rate for identifying specific causes, typically 5-20% across common evaluations like blood and urine cultures or CXR, underscoring the need for targeted rather than routine testing to avoid unnecessary interventions.^[34] Serial monitoring of inflammatory markers, such as CRP every 48-72 hours, is essential for tracking resolution or progression, integrating with clinical context for optimal interpretation.^[1]

Management

Initial Evaluation and Supportive Care

The initial evaluation of postoperative fever begins with close observation of the patient's vital signs, typically monitored every 4 hours on general surgical wards to detect changes in temperature, heart rate, blood pressure, and oxygen saturation.^[35] This protocol allows for early identification of stability or deterioration without immediate invasive interventions. In stable patients with fever below 39°C, antipyretics such as acetaminophen at a dose of 650 mg every 6 hours can be administered for symptomatic comfort, as it effectively reduces temperature without addressing underlying causes.^[36]^[37] Supportive measures emphasize maintaining hydration and nutrition to support recovery and immune function. Intravenous fluids should be provided if signs of dehydration are present, guided by assessment of intake/output and clinical status, to prevent complications like hypotension.^[1] Early enteral feeding, initiated within 24-48 hours postoperatively when tolerated, bolsters nutritional status, enhances gut immunity, and has been shown to shorten hospital stays compared to delayed feeding.^[38] Non-pharmacologic approaches focus on comfort and temperature modulation without aggressive cooling. Cooling blankets or tepid sponging with water at 32-35°C can be used adjunctively to lower temperature gradually, particularly in patients uncomfortable from fever, while avoiding methods that cause shivering.^[39] Aspirin should be avoided in postoperative patients at risk of bleeding due to its antiplatelet effects.^[1] Escalation is warranted for persistent fever exceeding 39°C lasting more than 24 hours or accompanied by hemodynamic instability, such as tachycardia or hypotension, prompting multidisciplinary consultation with infectious disease specialists or surgeons to guide further assessment.^[40] Evidence indicates that supportive care alone resolves the majority of benign postoperative fevers, particularly those occurring within the first 48 hours, which often stem from surgical inflammation rather than infection, thereby reducing overall hospital length of stay.^[41]^[38]

Cause-Specific Interventions

Once the underlying cause of postoperative fever has been identified through diagnostic evaluation, management shifts to targeted interventions that address the specific etiology, aiming to resolve the fever and prevent complications. Source control, such as drainage of abscesses or removal of foreign bodies, is a cornerstone of treatment for infectious causes and is associated with high success rates exceeding 90% when performed promptly alongside antimicrobial therapy.^[42] For infectious causes, empiric antibiotic therapy is initiated based on the suspected site and risk factors, with de-escalation guided by culture results to minimize resistance and adverse effects. In surgical site infections (SSIs), particularly superficial ones following clean procedures, a brief course of systemic antibiotics is recommended if systemic signs are present, such as cefazolin for methicillin-sensitive Staphylococcus aureus (MSSA) or vancomycin for methicillin-resistant S. aureus (MRSA) in high-risk patients.^[43] Drainage via incision and suture removal is essential for purulent collections, often resolving fever within 48-72 hours of intervention.^[1] For urinary tract infections (UTIs), common in catheterized patients, empiric therapy with ciprofloxacin or trimethoprim-sulfamethoxazole is used, adjusted per urine culture sensitivities, with a typical duration of 7-14 days depending on complexity.^[1] The Infectious Diseases Society of America (IDSA) guidelines emphasize early source control and tailored antimicrobials for SSIs, recommending extension of therapy beyond 5 days if clinical improvement is lacking.^[43] Defervescence is monitored closely, with persistent fever prompting reassessment for resistant pathogens or inadequate drainage. Noninfectious causes require discontinuation or modification of the offending agent to achieve rapid resolution. Drug-induced fever, often due to antibiotics or other medications, is managed by promptly stopping the suspected agent, with fever typically abating within 48-72 hours; supportive care is continued until confirmation by exclusion of other etiologies.^[1] For thromboembolic events like deep vein thrombosis (DVT) or pulmonary embolism (PE), anticoagulation with low-molecular-weight heparin (LMWH), such as enoxaparin, is initiated following confirmatory imaging, with a minimum duration of 3 months per American Society of Hematology (ASH) guidelines, adjusted for ongoing risk factors.^[44] This approach reduces recurrence risk by over 80% in postoperative settings.^[1] Surgical or procedural interventions are reserved for persistent or severe cases tied to operative complications. Re-exploration of the surgical site is indicated for deep SSIs or abscesses not amenable to percutaneous drainage, allowing for debridement and culture-directed therapy, often leading to fever resolution within 72 hours.^[1] For refractory atelectasis contributing to fever, bronchoscopy may be employed to clear mucus plugs or secretions, particularly if conservative measures like incentive spirometry fail, with success in re-expansion reported in most cases.^[45] Overall, most infectious treatments span 7-14 days, with clinical response assessed by defervescence and normalization of inflammatory markers within 48-72 hours; failure to improve warrants infectious disease consultation.^[43]

Prevention

Preoperative Measures

Preoperative measures focus on optimizing patient health, administering targeted prophylaxis, conducting relevant screenings, and providing education to reduce the incidence of surgical site infections (SSIs), a primary cause of postoperative fever. These strategies address modifiable risk factors such as comorbidities and microbial colonization, thereby lowering the overall risk of infectious complications following surgery. Patient optimization begins with smoking cessation, recommended at least 4 weeks prior to surgery, as supported by guidelines, with longer periods potentially offering greater benefits in reducing the incidence of postoperative complications, including wound infections and pulmonary issues, compared to continued smoking.^[46] Glycemic control is equally critical, particularly for diabetic patients, with a target preoperative HbA1c level below 7% linked to significantly lower SSI rates; for example, one study in diabetic patients found SSI rates of 35.3% for levels above 7% compared to 0% below this threshold, due to impaired immune response and wound healing.^[47] Nutritional screening is another key component, evaluating serum albumin levels to identify malnutrition; hypoalbuminemia (below 3.5 g/dL) independently predicts higher SSI risk through mechanisms like reduced collagen synthesis and immune function.^[48] Antibiotic prophylaxis plays a central role in SSI prevention for clean and clean-contaminated procedures, involving a single intravenous dose of cefazolin administered 30-60 minutes before incision to achieve bactericidal concentrations at the surgical site, with redosing recommended for procedures exceeding 4 hours or involving significant blood loss.^[49] This approach, guided by evidence-based protocols, has been shown to reduce SSI incidence by approximately 50% when appropriately timed and selected.^[50] Screening for potential infection sources includes nasal decolonization with mupirocin ointment applied twice daily to each nostril for 5 days prior to surgery in patients identified as Staphylococcus aureus carriers, particularly for high-risk procedures like orthopedic or cardiothoracic surgery, which can decrease S. aureus-related SSIs by up to 57%.^[51] Additionally, any preoperative urinary tract infection (UTI) should be treated with targeted antibiotics before elective surgery, as untreated UTIs are associated with increased postoperative morbidity, including a higher likelihood of SSI due to hematogenous bacterial spread.^[52] Patient education reinforces these measures by counseling individuals on personal hygiene practices, such as full-body showering with soap or antiseptic the night before surgery to reduce skin bacterial load, and early mobility plans to promote circulation and prevent stasis-related infections.^[49] Such interventions empower patients to participate actively in prevention, contributing to overall SSI risk reduction when combined with clinical strategies.^[53]

Intraoperative and Postoperative Strategies

Intraoperative strategies play a crucial role in minimizing the risk of postoperative fever by reducing the potential for surgical site infections (SSIs) and other complications. Adherence to strict aseptic technique throughout the procedure, including proper sterilization of instruments, maintenance of a sterile field, and use of barriers to prevent microbial contamination, has been shown to significantly lower SSI rates. ^[54] ^[1] Maintaining normothermia during surgery is another key measure, as intraoperative hypothermia impairs immune function and tissue perfusion, increasing susceptibility to infections that can manifest as postoperative fever. Forced-air warming devices, targeting core temperatures near 37°C, effectively prevent hypothermia and have been associated with reduced SSI incidence in randomized trials. ^[55] ^[56] Minimizing tissue trauma through precise surgical techniques, such as laparoscopic approaches when feasible, limits inflammatory responses and cytokine release that contribute to early postoperative fever. ^[41] Additionally, keeping procedure times as short as possible is essential, since prolonged operative duration—often exceeding 2-3 hours—correlates with higher SSI risk due to extended exposure and potential contamination. ^[57] Postoperative strategies focus on vigilant monitoring and interventions to avert infections and thromboembolic events that may lead to fever. Early mobilization, initiated on postoperative day 1 (POD1) for eligible patients, promotes circulation and reduces stasis, thereby decreasing deep vein thrombosis (DVT) risk; studies indicate it can lower DVT incidence by up to 60% when combined with other measures. ^[58] Incentive spirometry, performed every hour while awake, encourages deep breathing to prevent atelectasis and postoperative pneumonia, common fever triggers, with evidence supporting its role in reducing pulmonary complications. ^[59] Prompt removal of indwelling urinary catheters within 24 hours postoperatively is recommended to minimize catheter-associated urinary tract infections (CAUTIs), which account for a notable portion of early fevers. ^[60] For DVT prophylaxis, subcutaneous heparin (e.g., low-molecular-weight forms like enoxaparin) is widely used in moderate- to high-risk patients, halving VTE events without excessively increasing bleeding risk. ^[61] Wound care protocols emphasize sterile occlusive dressings applied immediately post-closure, left intact for at least 48 hours unless soiled or saturated, as routine changes can introduce contaminants and elevate SSI risk. ^[62] Ongoing surveillance for SSIs involves daily inspection for erythema, drainage, or dehiscence, enabling early detection without unnecessary interventions. ^[63] Broader infection control measures, such as rigorous hand hygiene by all staff and implementation of bundle protocols, further mitigate fever risks. For instance, ventilator-associated pneumonia (VAP) prevention bundles in ICU settings—including head-of-bed elevation, oral care, and daily sedation interruption—have demonstrated up to 30-50% reductions in VAP rates, indirectly lowering postoperative fever incidence in recent analyses. ^[64] ^[65] These multifaceted approaches, when consistently applied, enhance overall recovery and reduce fever-related morbidity.

Prognosis and Complications

Expected Outcomes

Most postoperative fevers are benign and resolve spontaneously within 72 hours without requiring specific intervention.^[1] These cases, often attributable to physiologic responses like inflammation from surgical trauma or atelectasis, typically lead to full patient recovery within 1-2 weeks as part of the overall postoperative healing process.^[1]^[3] Recovery is influenced by several key factors, including the promptness of diagnosis and the underlying etiology. Early identification and management can significantly shorten fever duration compared to delayed evaluation, where persistent symptoms may extend beyond a week in cases of infectious causes.^[3]^[6] Low-virulence etiologies, such as atelectasis or transient inflammatory responses, generally resolve more rapidly than those involving antibiotic-resistant infections, which may prolong the febrile period.^[1] Outcomes vary by surgery type, with higher complication risks in procedures like cardiovascular or neurosurgery, and patient factors such as comorbidities or immunosuppression.^[1]^[66] Clinically, postoperative fever often extends hospital length of stay by 2-5 days on average, depending on the surgical context and patient factors.^[6] Readmission rates following postoperative fever are generally low and comparable to non-febrile patients, typically around 10-15% overall.^[67] Long-term chronic sequelae are rare, with follow-up monitoring of C-reactive protein (CRP) levels commonly used to confirm resolution and normalization, indicating successful recovery.^[1] Most cases resolve with timely supportive care and cause-specific treatment, as noted in recent reviews.^[6]^[68]

Potential Complications

Untreated postoperative infections, particularly those arising from surgical sites, urinary tract, or respiratory sources, can escalate to sepsis or septic shock, marked by systemic inflammatory response and organ hypoperfusion, including elevated lactate levels greater than 2 mmol/L despite fluid resuscitation.^[1]^[5] This progression carries a mortality rate of 20% to 40%, influenced by factors such as patient age and the underlying pathogen.^[69]^[70] Severe postoperative fever often precipitates multi-organ dysfunction, with pneumonia-related infections leading to acute respiratory distress syndrome (ARDS), characterized by bilateral infiltrates and hypoxemia requiring mechanical ventilation.^[71] Urosepsis, a common postoperative complication from urinary tract infections, frequently results in acute renal failure due to hypoperfusion and direct nephrotoxic effects, potentially necessitating dialysis.^[72]^[73] Similarly, deep wound infections can cause wound dehiscence, where surgical incision edges separate, increasing risks of evisceration and secondary infections with mortality up to 40% in severe cases.^[74]^[75] Postoperative fever, often linked to immobility and hypercoagulability, heightens the risk of thromboembolic events, where deep vein thrombosis (DVT) can progress to pulmonary embolism (PE), with an incidence of 1% to 2% for PE in high-risk surgeries such as orthopedic or abdominal procedures without prophylaxis.^[76]^[77] Additional sequelae include prolonged mechanical ventilation due to respiratory complications exacerbating fever, often extending ICU stays and increasing resource utilization.^[78] Empiric antibiotic overuse prompted by persistent fever fosters antimicrobial resistance, complicating future treatments and elevating infection recurrence rates.^[79]^[80] Fever persisting beyond 7 days is associated with increased risk of severe complications, with elderly patients and those with comorbidities facing amplified vulnerability due to diminished physiologic reserves.^[81]^[82]^[83]

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