Postoperative Fever in the Digestive Oncology Patient

Definition

Fever above 38 °C is a common phenomenon in the first few days after any major surgery. In many cases, it is caused by the inflammatory response triggered by surgical aggression, which subsides spontaneously. However, fever can also be indicative of a complication. The differential diagnosis should include infectious and non-infectious conditions. In patients in the postoperative period following oncologic surgery, the tumor process itself may also cause the onset of fever.

1. Introduction

Postoperative fever is a common clinical finding following gastrointestinal (GI) oncologic surgery, with reported incidence rates ranging from 14% to 91%, depending on the type of procedure and patient population. While fever in the immediate postoperative period is often benign and self-limiting, it can also be an early indicator of serious complications such as anastomotic leaks, intra-abdominal abscesses, or surgical site infections. In oncologic patients, however, the interpretation of postoperative fever is particularly complex due to the interplay of cancer-related inflammation, immunosuppressive therapies, and altered physiological responses. These factors necessitate a more nuanced diagnostic approach to avoid both under- and over-treatment [1,2,3].

Patients undergoing GI cancer surgery often present with unique immunological and metabolic profiles that influence their postoperative course. Immunosuppression—whether due to chemotherapy, malnutrition, or the tumor itself—can mask typical signs of infection, making fever one of the few early warning signs of complications. Additionally, tumor-related fever, driven by cytokine release or necrotic tumor tissue, may mimic infectious processes without an underlying microbial cause. This overlap complicates clinical decision-making, as standard fever workups may yield inconclusive results. Therefore, distinguishing between benign postoperative fever, infection, and tumor-related inflammation is critical for timely and appropriate management in this vulnerable population [1,2,3].

2. Pathophysiology of Postoperative Fever

An individual’s normal temperature varies by one degree around 37 °C. It has a circadian variation, being lower in the morning and higher in the evening. Fever is considered to be a temperature higher than 38 °C in three determinations, at least one hour, or the presence of a temperature greater than or equal to 38.5 °C on one occasion [1].

The presence of exogenous and/or endogenous pyrogens provokes a febrile response. This response is a complex physiological reaction to illness involving cytokine-mediated temperature elevation, the generation of acute-phase reactants, and the activation of numerous immune, endocrine, and physiological systems [1,2,3].

Postoperative fever is a common occurrence after surgery, and recent studies have provided insights into its primarily inflammatory nature rather than infectious causes. The inflammatory response can be triggered by tissue injury, surgical stress, and the release of cytokines (IL-1, IL-6, TNF alpha, and IFN gamma). IL-6 has been shown to have the strongest association with the onset of postoperative fever. Cytokines are released in response to tissue damage, but are not necessarily indicative of infection. The magnitude of the injury correlates with the degree of fever that develops. Genetic factors also influence cytokine release in response to the damage. In infectious causes of fever, bacterial endotoxins and exotoxins stimulate cytokine release, while non-steroideal anti-inflammatory drugs (NSAIDs) and glucocorticoids reduce this cytokine release and thus reduce the magnitude of fever [2,3]. In contrast, in clean and clean-contaminated surgeries, non-infectious fever is more frequent than infectious fever. The incidence of postoperative fever was found to be 14%, with 81% being non-infectious. Factors such as prolonged operation time, a history of asthma, and certain surgical techniques can increase the likelihood of postoperative fever. The insights from recent studies emphasize the importance of distinguishing between infectious and non-infectious causes to optimize postoperative care. This understanding is crucial for guiding clinical management and reducing unnecessary antibiotic use [4,5].

Tumor pathology is itself a cause of fever (called fever of unknown origin when there is no apparent cause beyond the tumor process) and occurs in 5–56% of cancer patients. Therefore, in patients undergoing oncological surgery, not only postoperative complications should be considered a cause of fever, but the tumor process itself can also contribute significantly, and should therefore be a cause to be included in the differential diagnosis of postoperative fever [6]. Several factors underlie the pathophysiology of tumoral fever, highlighting a complex interaction of various physiological systems. Differentiating tumoral fever from other causes of fever, such as infections or drug reactions, is crucial. This requires extensive diagnostic studies to exclude identifiable causes before suspecting tumoral fever. In some tumors, such as breast cancer, fever can be the first sign of disease recurrence or progression, often associated with new metastases. Tumoral fever can also present as intermittent fever, which is less common than continuous fever [7].

3. Timing of Fever

The timing of postoperative fever is a critical factor in distinguishing between benign inflammatory responses and potentially serious complications. Fever occurring within the first 48 to 72 h after surgery is often attributed to the normal physiological response to surgical trauma and tissue injury. However, fever that arises beyond this window, or that persists or worsens, may signal infection, anastomotic leak, or other postoperative complications. In oncologic patients, particularly those who are immunocompromised, the timing and pattern of fever must be interpreted with caution, as atypical presentations are common and may delay diagnosis if not carefully evaluated.

The timing of the onset of fever is one of the most important factors in the differential diagnosis of the etiology of postoperative fever. Depending on the time of onset, it can be divided into [8,9,10,11,12,13]:

• Immediate (first hours after surgery):

The main causes of fever in this period are medications administered in the perioperative period, infections or trauma present prior to surgery, and malignant hyperthermia. Drug reactions include mainly antibiotics and blood products. They are often accompanied by arterial hypotension and skin rash. Malignant hyperthermia typically presents within 30 min after administration of the triggering agent (inhalational anesthesia, succinylcholine) and manifests with hypercarbia as the first sign.

Fever secondary to the trauma of surgery resolves spontaneously in 2–3 days.

• Acute (First week after surgery):

In this period nosocomial infections (Surgical Site Infection (SSI), intravascular catheter infection, respiratory infection, and urinary tract infection) are typical. There are also non-infectious causes, such as pancreatitis, acute myocardial infarction, pulmonary thromboembolism, or thrombophlebitis.

• Subacute (between one week and one month after surgery):

SSI is one of the most frequent causes of fever in this period, even in patients who have been discharged from hospital. Long-term central venous catheters, antibiotic-associated diarrhea attributed to Clostridium difficile, and certain medications prescribed for the postoperative period, such as heparins or anti-H2, may also be causes. Thromboembolic phenomena are also etiological agents in this time frame. Patients requiring a prolonged stay in the ICU are very prone to nosocomial infections due to central intravascular catheter, respiratory, and urinary tract infections.

• Late (after the first month after surgery):

Most cases of late fever are due to infectious causes of viral origin (cytomegalovirus, hepatotropic viruses, and human immune deficiency virus), due to indolent bacteria (coagulase-negative Staphylococcus), due to the presence of prosthetic material, and occasionally due to parasites. Infective endocarditis may also cause fever in this period.

Fever associated with the oncologic process may occur in all the phases of the postoperative course. It is especially more frequent when tumoral fever was present preoperatively and when R0 radicality is not achieved.

The timing of the fever and its most frequent etiologies are summarized in

Table 1. Timing of fever and its etiologies. SSI: Surgical site infection.

Timing	Etiology
Immediate	Drug reactions Infections or trauma present prior to surgery Malignant hyperthermia
Acute	Nosocomial infections (SSI, intravascular catheter infection, respiratory infection, urinary tract infection) Non-infectious causes (pancreatitis, acute myocardial infarction, pulmonary thromboembolism, thrombophlebitis)
Subacute	Central venous catheters Urinary or respiratory infections Diarrhea caused by Clostridium difficile Medication (heparins, H2 blockers) Thromboembolic phenomena
Late	Infectious: - Virus - Bacteria - Parasites - Endocarditis - Infection of prosthetic material Tumoral fever

.

4. Etiology

The etiology of postoperative fever is multifactorial and can range from benign, self-limiting causes to life-threatening complications. In the early postoperative period, fever is often a result of the body’s inflammatory response to surgical trauma, including cytokine release and tissue injury. However, other etiologies must be considered depending on the timing, severity, and associated clinical signs. These include infectious causes such as surgical site infections, pneumonia, urinary tract infections, and catheter-related bloodstream infections, as well as non-infectious sources like drug reactions, blood transfusions, deep vein thrombosis, and tumor-related fever. The accurate identification of the underlying cause is essential for guiding appropriate management and avoiding unnecessary interventions.

The most frequent etiologies involved in the development of postoperative fever include:

• Infection:

Includes SSI, pneumonia, urinary tract infection, and vascular catheter infection. Nosocomial bacteria and fungi are involved. The microorganisms involved are from endogenous flora and skin flora, but changes in flora due to prolonged hospitalization and antibiotic therapy are the cause of infection by resistant microorganisms. Other less frequent postoperative infections include sinusitis, otitis media, bacterial meningitis, and alithiasic cholecystitis. The retention of foreign material (i.e., retained gauze) or infected prosthetic material can also be a source of persistent fever [14,15,16,17].

• Drugs:

They represent one of the main causes of postoperative fever. Antibiotics and heparins are most commonly implicated [18].

• Malignant hyperthermia:

Malignant hyperthermia is a hereditary disorder manifesting as hypermetabolic conditions during general anesthesia. These patients have alterations in skeletal muscle receptors, which allow excessive calcium accumulation in the presence of certain triggering agents [18,19].

• Transfusion of blood products:

Fever may result from immunologic responses to transfused blood components [20].

• Endocrine causes:

Hyperthyroidism may cause postoperative fever. Adrenal insufficiency due to bilateral adrenal infarction secondary to coagulopathy may also cause fever [21].

• Atelectasis:

It is often a cause of fever of unknown origin. It consists of a lack of expansion of lung segments or lobes, due to a lack of deep inspirations. They are usually associated with poor postoperative pain control, which leads to a tendency to take shallow breaths. In these cases surfactant and other secretions, as well as pollutants in the inspired air, accumulate in the pulmonary alveoli and this lack of ventilation leads to their collapse. Often, this atelectasis, if not properly managed with respiratory physiotherapy and elimination of the cause of the atelectasis, can lead to pneumonia [22].

• Tumor fever:

Cancer patients may present with fever not associated with the surgical process. Therefore, it may be present before the operation and persist after it. On the other hand, surgical manipulation of the tumor may favor the release of tumor pyrogens and the onset of fever in the immediate postoperative period. However, it should be borne in mind that all cancer patients have a certain degree of immunosuppression, which makes them more susceptible to postoperative infectious complications. Fever of tumor origin should therefore be included in the differential diagnosis of postoperative fever in this type of patient, but other causes of fever derived from postoperative complications must first be ruled out [23].

Tumor-related fever and postoperative inflammation often coexist in patients undergoing GI oncologic surgery, creating significant diagnostic challenges. Tumor fever, typically mediated by cytokines released by malignant cells or the host immune response to the tumor, can persist into the postoperative period and mimic infectious or inflammatory complications. This overlap becomes particularly problematic when patients are also experiencing the expected inflammatory response to surgical trauma, which itself can cause transient fever. The clinical picture is further complicated in patients receiving chemotherapy or biologic agents, as these treatments can suppress typical signs of infection (e.g., leukocytosis) or induce fever as an adverse effect, blurring the distinction between drug-related, tumor-related, and infection-related fever.

In immunocompromised patients, especially those on cytotoxic chemotherapy or targeted biologics like immune checkpoint inhibitors, the febrile response may be blunted or atypical. For instance, neutropenic patients may not present with a robust fever despite serious infection, while others may experience fever due to cytokine release syndromes or immune reconstitution inflammatory syndrome (IRIS). These overlapping etiologies demand a careful and often multidisciplinary diagnostic approach, incorporating clinical context, imaging, microbiological cultures, and sometimes empirical treatment trials. Misattributing tumor fever to infection can lead to unnecessary antibiotic use, while overlooking a true infection in an immunosuppressed host can have fatal consequences. Thus, distinguishing among these causes is critical for optimizing outcomes in this vulnerable population.

• Inflammation secondary to surgical trauma:

Postoperative fever can frequently arise as a physiological response to the inflammatory cascade triggered by surgical trauma. Tissue injury during gastrointestinal oncologic procedures leads to the activation of the innate immune system, resulting in the release of pro-inflammatory mediators such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and prostaglandins. These mediators act on the hypothalamic thermoregulatory center, elevating the body’s set-point temperature and producing fever. This sterile inflammatory response is typically self-limiting and occurs within the first 48 to 72 h post-surgery. However, distinguishing this benign postoperative fever from early signs of infection or other complications is essential, particularly in oncologic patients, where overlapping symptoms may obscure the clinical picture [4,5].

5. Management of the Digestive Oncology Patient with Postoperative Fever

The management of postoperative fever in digestive oncology patients requires a careful, individualized approach due to the complex interplay of surgical stress, immunosuppression, and potential tumor-related factors. These patients often present with atypical signs of infection or inflammation, making early recognition and differentiation between benign postoperative responses and serious complications essential. A structured evaluation, including clinical assessment, laboratory tests, imaging, and consideration of recent treatments such as chemotherapy or biologics, is crucial to guide appropriate interventions. The prompt identification of the underlying cause not only improves outcomes but also helps avoid unnecessary antibiotic use and prolonged hospital stays in this vulnerable population.

Initially, chest X-ray, urine biochemical analysis, blood and urine cultures are not indicated for all patients with postoperative fever. Their necessity will depend on the clinical findings, evaluating the possible causes of this febrile state according to the time of the onset of fever. Among all the possibilities, there are five that should always be suspected:

• Respiratory pathology: pneumonia, atelectasis, or bronchial aspiration.
• Urinary and catheter-associated infection.
• Surgical site infection—initially incisional, subsequently organ space surgical site infection (OS-SSI).
• Thromboembolism.
• Drug-induced fever.

Once the above causes have been ruled out, and therefore the absence of postoperative complications, tumor fever can be considered among the aetiological factors of this fever of unknown origin [24,25].

6. Treatment

The treatment of postoperative fever involves a stepwise approach that begins with identifying the underlying cause, as management strategies vary significantly depending on the etiology. In many cases, especially within the first 48–72 h after surgery, fever may be due to a benign inflammatory response and may not require specific treatment beyond observation and supportive care. However, when infection or other complications are suspected, targeted interventions such as antimicrobial therapy, drainage of abscesses, or surgical revision may be necessary. In oncologic patients, special consideration must be given to immunosuppression and the possibility of tumor-related fever, which may not respond to antibiotics and instead require anti-inflammatory or antineoplastic therapies. Timely and accurate diagnosis is essential to guide appropriate treatment and avoid unnecessary interventions.

Although definitive treatment will depend on the identification of the cause and its specific treatment, there are a number of general measures that can be applied.

Some common approaches include:

• Hydration: When oral intake is possible, the patient must drink plenty of fluids to prevent dehydration, secondary to water loss through sweat.
• Cooling techniques: Apply cool compresses or take baths to help regulate body temperature.
• Medication: The antipyretic of choice should be Acetaminophen; non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen can also be used. In children, aspirin must be avoided.
• Withdrawal of non-essential medications and catheters may aid in identifying the fever’s etiology: In many cases, this measure already leads to the disappearance of fever within 24–48 h.
• Monitoring: Keep track of temperature changes and watch for signs of complications.

In most cases, mild fever does not require aggressive treatment, as it is part of the body’s natural defense mechanism. Fever control is necessary to improve the patient’s discomfort and reduce the psychological and metabolic stress of the febrile state. However, if the fever is persistent, very high, or accompanied by other symptoms, severe complications must be suspected [26].

The addition of antibiotics will depend on identifying the cause, bearing in mind that most postoperative fevers have a non-infectious etiology. It is true that in those patients admitted to the ICU after major surgery and in a situation of hemodynamic instability, it would be indicated to add broad-spectrum antibiotic treatment empirically after taking cultures, simply because of the possibility that the fever is of infectious origin and the seriousness of the situation does not suggest speculating on other causes.

In cases of fever or infectious origin, empirical antibiotics should be initially administered, fever may result from covering all the microorganisms most frequently involved in the type of infection suspected. Depending on the severity of the process and the patient’s risk factors, one type of antimicrobial agent or another will be prescribed, and the duration of the treatment will be estimated, using broader-spectrum antibiotics and longer treatments when nosocomial infections or multidrug-resistant agents are suspected, and in patients in a more serious condition. As soon as the source of the fever is identified or cultures are positive for a specific organism and its sensitivity is known, antibiotic treatment should be directed towards that source and the causative microorganism, if this is not correctly covered or the evolution of the patient is not adequate [27].

The other basic principle of fever of infectious origin consists of the control of the infectious focus. If there is an inserted foreign body (peripheral venous catheter, tube, prosthetic material, etc.). It is common for the infectious agents to remain lodged on this foreign body, favoring its proliferation and dissemination. For this reason, it is often necessary to remove these devices. In the case of probes or catheters, this may not be a great difficulty. However, in the presence of an implanted biomaterial prosthesis, its removal often implies a major surgical intervention and the removal of this material entails important postoperative functional consequences.

Moreover, the vascularization around the prosthetic material is also reduced, which reduces the local bioavailability of the prescribed antibiotic. The same phenomenon occurs in the presence of an organ cavity infection. The antibiotic does not reach sufficient concentrations on the nucleus of bacterial proliferation and therefore its bacteriostatic or bactericidal effect is reduced. Therefore, under these circumstances, the infectious focus must be drained by resection of an organ segment or evacuation of pus or other infected liquid. In addition, the infected cavity should be irrigated, which dilutes the bacterial concentration, thus facilitating the therapeutic action of the antibiotic. The drainage of the focus should initially be approached in the least invasive way possible, preferring percutaneous drainage guided by CT or ultrasound. If these fail or are not possible, surgical drainage of the focus should be chosen [28].

When a tumor fever is present, the administration of corticosteroids associated with NSAIDs (naproxen, diclofenac, or indomethacin) may be necessary. Corticosteroids and anti-inflammatory drugs help manage tumor fever through several mechanisms:

• Corticosteroids suppress the production of cytokines, which are key mediators of fever. They also inhibit prostaglandin E2 (PGE2) synthesis, reducing hypothalamic temperature regulation, and they modulate immune cell activity, decreasing inflammation and fever-related symptoms.
• Non-steroidal anti-inflammatory drugs block cyclooxygenase (COX) enzymes, preventing the formation of PGE2, which is responsible for fever generation. They also reduce vascular inflammation, improving circulation and lowering the fever.

Studies suggest that combining corticosteroids and NSAIDs can enhance fever control in patients with cancer-related inflammation [29].

7. Specific Considerations to OS-SSI

OS-SSI is one of the most frequent surgical complications and one of the most feared due to its high morbidity and mortality. Its early diagnosis is a challenge for the clinician, even more in cancer patients, whose immunosuppressed state significantly increases not only the incidence but also the severity of this complication, which can be minimized with early diagnosis and treatment [11].

OS-SSI can present as diffuse peritonitis, but it can also appear as a localized intra-abdominal abscess. In this case, early diagnosis may allow minimally invasive treatment, which improves the patient’s recovery, since surgery carries a high complication rate. However, in a patient with severe sepsis and peritonitis, the placement of a percutaneous drain would not be indicated, since this would result in insufficient control of the focus and would probably lead to persistence of the infection [12,13].

Better knowledge of the pathophysiology, together with a high index of clinical suspicion, will allow for the early recognition of the pathology, the establishment of appropriate and early treatment and a reduction in secondary morbidity and mortality.

Intra-abdominal abscesses are a localized form of OS-SSI. They are collections of pus, usually well-defined, arising from the introduction of enteric flora into usually sterile sites. Intra-abdominal abscesses are a consequence of the host immune and inflammatory response that confines and prevents the spread of intra-abdominal infection in the form of peritonitis. Infection is limited by the barriers formed by the omentum, inflammatory adhesions, and the adjacent viscera. The location of these abscesses will be determined by the focus of origin (primary site of contamination), mesenteric divisions and peritoneal recesses, the direction of flow of peritoneal fluid by gravity and pressure gradients within the peritoneal cavity. The microenvironment of the intra-abdominal abscesses makes the availability and efficacy of antibiotics suboptimal for a variety of reasons:

• Poor irrigation, resulting in reduced bioavailability of the antibiotic. As a result, the antibiotic concentration at the abscess site is inadequate and resistant bacterial strains are selected.
• Mechanical barriers (fibrin, detritus, or foreign bodies). The aim of drainage is to eliminate these barriers in order to optimize the action of the antibiotic.

Lack of proper drainage perpetuates the inflammatory process, weakens the host, worsens the nutritional status, and facilitates the spread of infection, favoring severe sepsis and septic shock [10,14].

7.1. Microbiology of OS-SSI

Most OS-SSIs are made up of mixed flora (aerobic and anaerobic organisms). The most frequently isolated aerobe is Escherichia coli and the anaerobe Bacteroides fragilis, which act synergistically. However, cultures may show fungi and other nosocomial pathogens such as Enterococcus spp. or Pseudomonas aeruginosa [1,14].

7.2. Clinical Features and Diagnosis

The presentation of OS-SSI is variable and non-specific. The most common findings are presented in

Table 2. Clinical symptoms, signs, and laboratory data present in OS-SSI.

Persistent Abdominal Pain with Localized Peritoneal Irritation.
Prolonged postoperative ileus.
Signs of systemic inflammation: fever spikes, tachycardia, leukocytosis.
Elevated C-reactive protein (CRP).
Hypoalbuminaemia.
Persistent polymicrobial bacteraemia.

:

Depending on the location, the clinical picture may vary. Subphrenic involvement, for example, may lead to pulmonary atelectasia In addition, analgesia, antibiotics, and pain from the surgical incision may mask some of the symptoms.

A fever presented in a week’s time should prompt the surgeons to consider assessing anastomotic leak with a contrast study or CT scan.

Delays in diagnosis and treatment result in inadequate cost in human and financial resources and increase the mortality rate [10,12,15].

• Laboratory data. Leukocytosis (although leukopenia may be found in patients with an inadequate immune response), anemia, plateletopenia, and altered liver profile are the main biochemical signs of infection. Elevation of acute phase reactants such as C-reactive protein (CRP), fibrinogen, procalcitonin, or erythrocyte sedimentation rate (ESR) may also be observed.
• Microbiology. Some patients have received previous antibiotics, which is the main risk factor for antimicrobial therapeutic failure due to inadequate treatment. Therefore, it is very important to obtain a sample for microbiological study, either from intraperitoneal fluid or blood, for Gram staining and culture.
• Plain abdominal X-ray. It may show non-specific signs that are useful to indicate further diagnostic tests. These include ileus, extraluminal gas, hydroaerial levels, effacement of the psoas line, or visceral displacement.
• Chest X-ray. In case of subphrenic or subhepatic involvement, pleural effusion, elevation of the hemidiaphragm, basal lung infiltrates, or atelectasis may be observed. Pneumoperitoneum may also be seen in cases of hollow viscera perforation.
• Computed tomography (CT). It is the test of choice for the diagnosis of OS-SSI (with an over 95% accuracy and a sensitivity and specificity of 95–97% and 94–95%, respectively). The administration of oral and/or rectal contrast allows the diagnosis of fistulas or anastomotic dehiscence. In contrast, intravenous contrast tends to concentrate in hypervascularized areas, such as inflamed bowel loops. Contrast administration is limited by the presence of ileus (oral contrast), contrast allergy, or renal insufficiency. The limitations of CT are related to non-portability, poor sensitivity for diagnosing abscesses between bowel loops, and the need for patient cooperation.

7.3. Antibiotic Treatment and Focus Control

Early diagnosis, appropriate antibiotic treatment, control of the focus, and supportive care are the basis for the treatment of any OS-SSI.

For adequate control of the intra-abdominal infectious focus there are two methods that have been extensively studied: percutaneous drainage (PD) and surgical drainage (SD). The safety and effectiveness of percutaneous drainage was first described in 1970 and has become an established procedure. Numerous studies have shown that PD is associated with longer survival than SD. However, the decision must be individualized for each patient and in critically ill patients with severe systemic repercussions, surgery is indicated. Currently, the laparoscopic approach is possible in most cases of OS-SSI, with adequate control of the infectious focus, but minimizing the surgical aggression of open surgery [1,10,16].

Principles of Antibiotic Treatment [30,31,32,33,34,35]

a.

Initiation prior to drainage of the abscess and termination when all signs of sepsis are normalized.

b.

Target mixed flora (aerobic and anaerobic), using combination therapy or a single broad-spectrum antibiotic, taking into account that this is a nosocomial infection.

c.

Administration of appropriate empirical treatment according to the patient’s risk factors for the involvement of micro-organisms with bacterial resistance.

d.

Empirical treatment directed by Gram staining–the presence of Gram-positive cocci, especially in patients previously treated with 3rd generation cephalosporins, should alert to the presence of Enterococcus spp. In the case of very severe patients, antibiotics active against E. faecium should be included (linezolid, daptomycin, vancomycin, tigecycline) and de-escalation in view of the microbiological results if adequate activity of beta-lactams is shown.

8. Conclusions

Postoperative fever in digestive oncology patients is a multifactorial phenomenon that requires a nuanced and timely diagnostic approach. While fever is often a benign response to surgical trauma, it can also signal serious complications such as infections, thromboembolic events, or drug reactions. The timing of fever onset plays a critical role in narrowing down potential causes, ranging from immediate drug reactions to late-onset infections or tumor-related fevers. Understanding the pathophysiology, including the role of cytokines and immune responses, is essential for differentiating between infectious and non-infectious etiologies. Moreover, the presence of tumor fever, particularly in patients with preoperative symptoms or incomplete tumor resection, must be considered once other causes are excluded.

Effective management hinges on a combination of clinical vigilance, appropriate diagnostic testing, and targeted therapeutic interventions. Empirical antibiotic therapy should be guided by clinical suspicion and adjusted based on microbiological findings, while non-infectious causes may require withdrawal of medications or supportive care. In cases of OS-SSI, early recognition and control of the infectious focus—preferably through minimally invasive techniques—are vital to improving outcomes. Ultimately, a multidisciplinary approach that integrates surgical, infectious disease, and oncologic expertise is key to optimizing care and reducing morbidity and mortality in this vulnerable patient population.