Clinical characteristics and prognostic factors of severe intra-abdominal infection due to gastrointestinal perforation: a retrospective cohort study

Abstract

Objective

Gastrointestinal perforation is a medical emergency. We aimed to explore clinical characteristics and prognostic factors in patients with severe intra-abdominal infection due to gastrointestinal perforation.

Methods

In this retrospective cohort study, we reviewed patients diagnosed with severe intra-abdominal infection due to gastrointestinal perforation between January 2020 and January 2025. Demographics, clinical information, laboratory test results, management approach, 28-day mortality, and 180-day survival rate were recorded. Through regression probability analysis, multivariate logistic regression, Kaplan-Meier survival analysis, and Cox regression, we systematically analyzed patient clinical characteristics and determined the variables impacting their prognosis.

Results

A total of 108 eligible patients were included, with a 28-day mortality rate of 24.1% and a 180-day survival rate of 59.3%. Smoking history, diabetes, cardiovascular disease, rheumatic immune disease, malignant tumors, presence of elevated procalcitonin, the Acute Physiology and Chronic Health Evaluation II score, Mannheim Peritonitis Index score, low serum albumin and low prealbumin, infection from the stomach and duodenum, and fungal infection were independent risk factors while empirical use of antifungal drugs was associated with reduced 28-day mortality (all p < 0.05). Diabetes (p = 0.047), malignant tumors (p = 0.016), initial serum albumin level below 30 g/L, prealbumin level below 300 mg/L, infection source control time exceeding 12 h (p < 0.001), and enteral nutrition initiation time exceeding 6 days (p = 0.001) were independent risk factors for 180-day survival status. Compared with patients whose infection originated from the jejunum, ileum, cecum, or colon, infection from the stomach and duodenum was an independent risk factor for 180-day survival status.

Conclusion

Patients with severe intra-abdominal infection due to gastrointestinal perforation had poor prognosis. Multiple variables were identified to be associated with 28-day mortality and 180-day survival. Early infection source control, appropriate enteral nutrition initiation could improve prognosis.Early and timely empirical antifungal treatment in addition to other necessary interventions might be considered in these patients.

Introduction

Severe intra-abdominal infection (SIAI) is a medical emergency. Affected patients commonly have systemic inflammatory response, characterized by sepsis or septic shock with rapid progress to multiple organ dysfunction. Despite recent advancements in diagnostic techniques, treatment methods, and critical care management, the in-hospital mortality rate of SIAI patients remained persistently high, from 32.0% and reaching 49% in the absence of appropriate timely and effective intervention [1–3]. Approximately 33.2% of intra-abdominal infections are attributed to gastrointestinal perforation [4], with reported mortality rates ranging from 30% to 50% in this patient population [5]. When the condition progresses to SIAI, the prognosis deteriorates rapidly and becomes substantially more severe [6, 7], thus posing a serious threat to public health [8].

The gastrointestinal tract is comprised of multiple segments, including the stomach, duodenum, jejunum, ileum, cecum, and colon. Microbial flora varies significantly across these different segments. Meanwhile, the pathogenic bacteria involved in SIAI are highly complex. Perforations occurring throughout the gastrointestinal tract result in distinct microbial profiles and subsequent diverse clinical outcomes [9]. This high degree of heterogeneity makes the diagnosis and management of perforation-induced SIAI particularly challenging [10, 11]. Understanding the clinical characteristics of perforation-induced SIAI and identifying risk factors for poor prognosis can provide evidence-based references for precise and individualized treatment recommendations.

We performed this retrospective review of patients in a tertiary grade-A hospital in China over a five-year period (2020–2025). We analyzed the data on SIAI patients with the aim to identify the clinical characteristics and risk factors associated with poor prognosis, with the ultimate goal to improve patient prognosis and reduce mortality and outline new directions for future research.

Materials and methods

Study design and participant selection

The present study was a single-center retrospective cohort study to review patients who were admitted into the First Affiliated Hospital of Fujian Medical University, China, from January 2020 to January 2025. The study protocol was approved by the hospital ethics committee (approval number 2025 − 391). The informed consent was waived due to the retrospective study design.

The inclusion criteria were patients with (1) age ≥ 18 years old; (2) a diagnosis of gastrointestinal perforation based on computed tomography scan imaging, together with a comprehensive evaluation of the patient’s medical history, symptoms, signs, and laboratory test results [12]; and (3) SIAI defined as when a patient had intra-abdominal infection and an Acute Physiology and Chronic Health Evaluation II (APACHE II) score of > 10 points and evidence of sepsis [13, 14].

The exclusion criteria were patients with (1) Esophageal perforation, intestinal fistula, anastomotic fistula, or diseases where the full thickness of the digestive tract wall is not damaged but digestive juices enter the peritoneal cavity (such as diverticulitis with minor perforation, perforation of the digestive tract reaching the serosal layer but without perforation, and local leakage due to tumor infiltration of the digestive tract, etc.); (2) less than 24 h in intensive care unit (ICU); (3) negative bacterial smears and cultures in blood, peritoneal drainage fluid, tissue culture, and diagnostic peritoneal puncture; or (4) patients that withdrew from treatment.

Data collection

Medical records were reviewed to retrieve information on demographics, weight, height, smoking and alcohol history, comorbidities, source of infection, pathogens, laboratory test results, sequential organ failure assessment (SOFA) and APACHE II score on the first day of diagnosis, Mannheim Peritonitis Index (MPI) score on the first day after surgery, and management approaches. In addition, time to control infection source (time from SIAI diagnosis to surgical intervention, including surgery, laparoscopic treatment, puncture, drainage, etc.), time to antibiotic intervention (time from SIAI diagnosis to antibiotic use), antibiotics (empirical anti-Gram-positive bacteria and empirical anti-fungal), fluid volume within 3 h after SIAI diagnosis (including crystalloid, colloid, and blood products).

The study outcomes include the duration of mechanical ventilation, length of ICU stay, length of hospital stay, 28-day mortality rate, and 180-day survival rate.

Statistical analysis

Statistical analysis was conducted using SPSS 26.0 software (SPSS, IBM, USA). Patients were assigned to survival group and death group, depending on the 28-day mortality. Continuous variables that followed a normal distribution were expressed as mean ± standard deviation and the significance of difference was assessed using t-tests. Continuous variables that did not follow a normal distribution were expressed as median (interquartile range) and compared using rank sum tests. The Chi-squared test was used to determine the significance of difference between categorical variables. Survival curves were plotted using the Kaplan-Meier method, and differences between groups were compared using the log-rank test. The median survival time and 95% confidence interval (CI) were reported. The analysis of the impact of multiple factors on patient prognosis was conducted using Cox regression forest plots; hazard ratios (HR) and 95% CI were reported. Logistic regression was employed to analyze the risk factors associated with mortality; odds ratios (OR) and 95% CI were reported. A p < 0.05 was considered statistically significant.

Results

We reviewed 1,604 patients with intra-abdominal infections. After considering inclusion and exclusion criteria, a total of 108 SIAI patients due to gastrointestinal tract perforations were included in the analysis, with a 28-day mortality rate of 24.1% and a 180-day survival rate of 59.3% (Fig. 1).

Fig. 1.

Patient selection flowchart. ICU, intensive care unit; SIAI, severe intra-abdominal infection

Characteristics associated with 28-day mortality

Table 1; Fig. 2 show that the 28-day mortality rate of enrolled patients was associated with multiple factors. Patients with comorbidities such as smoking history, diabetes, cardiovascular disease, rheumatism and immune diseases, or malignant tumors had a significantly increased risk of 28-day mortality. Elevated PCT, APACHE II score, and MPI score were also correlated with the 28-day mortality rate, whereas high serum albumin and prealbumin levels were associated with a significantly decreased 28-day mortality rate.

Table 1.

Clinical characteristic comparisons between survival and death group in SIAI patients due to gastrointestinal perforation

Characteristics	Survival group (n = 82)	Death group (n = 26)	t/χ2/Z	p
Sex, n (%)				0.782
Male	56 (68.3)	17 (65.4)	0.076
Age, years, median (IQR)	59 (48,71)	67.5 (54.5,78)	-1.934	0.053
BMI, kg/m2,median (IQR)	23.8 (2.4,29.5)	23.0 (21.3,25.8)	-0.841	0.400
Smoke, n (%)	32 (39.0)	19 (73.1)	9.185	0002
Alcohol, n (%)	31 (37.8)	11 (42.3)	0.168	0.682
Comorbidities, n (%)
Diabetes	8 (9.8)	7 (26.9)	4.864	0.027
Cardiovascular diseases	8 (9.8)	12 (46.1)	9.183	0.002
Chronic kidney disease	13 (15.9)	5 (19.2)	0.162	0.687
Chronic liver disease	19 (23.2)	3 (11.5)	1.647	0.199
Rheumatic immune diseases	5 (6.1)	5 (19.2)	4.053	0.044
Malignant tumor	6 (7.3)	8 (30.8)	9.623	0.002

BMI Body mass index, IQR Interquartile range, SIAI Severe intra-abdominal infection

Fig. 2.

Regression probability plot of different measurements associated with mortality in patients with severe intra-abdominal infection due to gastrointestinal perforation

Table 2 shows that the 28-day mortality rate varies depending on the source of infection (p = 0.027). Pairwise comparisons revealed that the 28-day mortality rate of patients with infection from the stomach and duodenum was significantly higher than that of the small intestine (jejunum, ileum, cecum) (p = 0.029) and the colon and rectum (p = 0.024), while there was no statistically significant difference in the 28-day mortality rate between small intestine, colon, and rectum sources of infection (p = 0.959). In terms of etiology, the 28-day mortality rate was higher in patients with mixed infections compared to those with single Gram-negative, Gram-positive bacterial, or fungal infections (p = 0.049). Additionally, the presence of fungal infection (p = 0.002) or Gram-positive bacterial infection (p = 0.039) significantly increased the risk of 28-day mortality. Among treatment-related factors, both the time to control the source of infection (p = 0.037) and the delay in initiating enteral nutrition (p = 0.001) were associated with an increased 28-day mortality rate. There was no statistically significant difference in length of hospital stay and duration of mechanical ventilation between the survival and death groups (p > 0.05) (Table 3).

Table 2.

Infection-related and laboratory test result comparisons between survival and death group in SIAI patients due to gastrointestinal perforation

Characteristics	Survival group (n = 82)	Death group (n = 26)	t/χ2/Z	p
Source of infection, n (%)	7.1870.027
Stomach and duodenum	21 (25.6)	14 (53.8)
Ileum, jejunum, cecum	30 (36.6)	6 (23.1)
Colorectum	31 (37.8)	6 (23.1)
Pathogen, n (%)	7.8560.049
Only Gram-negative bacteria	39 (47.6)	10 (38.5)
Only Gram-positive bacteria	12 (14.6)	0 (0)
Only Fungus	5 (6.1)	1 (3.8)
Mixed infection	26 (31.7)	15 (57.7)
Gram-negative bacteria	65 (79.3)	24 (92.3)	2.350	0.128
Gram-positive bacteria	59 (28)	13 (50)	4.280	0.039
Fungus	6 (7.3)	8 (30.8)	9.623	0.002
Antibiotics, n (%)
Empirical anti-Gram-positive bacteria	34 (41.5)	7 (26.9)	1.772	0.183
Empirical anti-fungus	22 (26.8)	2 (7.7)	4.183	0.041
Timing for source control, hours, median (IQR)	14 (7,25.3)	18.5 (37,32.3)	-2089	0.037
Management, n (%)
Laparoscopy	18 (21.2)	5 (21.7)	0.003	0.953
Ultrasound-guided needle aspiration and drainage	56 (65.9)	15 (65.2)	0.004	0952
CT-guided puncture and drainage	13 (15.3)	4 (17.4)	0.060	0.806
Exploratory laparotomy	14 (16.5)	3 (13.0)	0.160	0.689
Antibiotic administration time, hours, median (IQR)	1 (1,2)	1 (1,2.25)	-0.016	0.987
Fluid resuscitation volume within 3 h, mL, median (IQR)	1,000 (600,1,300)	875 (687.5,1,125)	-1.934	0765
Crystalloid volume, mL, median (IQR)	725 (500,1,000)	800 (500,1,000)	-0.007	0.994
Artificial colloid, mL, median (IQR)	0 (0,50)	0 (0,0)	-0.855	0.393
Albumin volume (4%), mL, median (IQR)	0 (0,50)	0 (0,50)	-0665	0.506
Blood product volume, mL, median (IQR)	0 (0,100)	0 (0,100)	-0.143	0.886
Norepinephrine, µg/kg·min, median (IQR)	0.5 (0.1,1.0)	0.2 (0.1,1.1)	-0.476	0.634
Laboratory tests
PCT, ng/mL, median (IQR)	23.1 (3.9,67.3)	70.5 (31.5,86.5)	-3116	0.002
CRP, mg/L, median (IQR)	101 (67.1,155.8)	140.14 (67.2,193.0)	-0.891	0.373
Serum albumin, g/L, M ± SD	41.2 ± 6.0	36.1 ± 8.0	3.455	< 0.001
Prealbumin, mg/L, M ± SD	323.7 ± 52.3	296.4 ± 59.1	2.246	0.027
Total bilirubin, µmol/L, median (IQR)	41.1 (24.5,108.7)	37.9 (26.4,109.2)	-0.075	0.940
Serum creatinine, µmol/L, median (IQR)	241 (151.3,324.0)	252 (193.3,323.5)	-0.223	0.824
Blood urea nitrogen, mmol/L, M ± SD	10.5 ± 3.8	10.4 ± 3.9	0.067	0.947
Neutrophil ratio, %, median (IQR)	89.8 (84.8,91.8)	91.2 (84.3,94.4)	-0.996	0.319
Hemoglobin, g/L, M ± SD	81.3 ± 17.1	85.7 ± 22.9	-1.056	0.294
Platelet, x 109/L, median (IQR)	111 (62.8,152.8)	113 (41.0,187.5)	-0.036	0.971
Clinical measurements, median (IQR)
SOFA	14 (12.0,15.3)	13 (11.8,16.0)	-0.587	0.557
Respiration disorder	3 (2,3)	3 (1,3)	-1.815	0.069
Coagulation disorder	1 (0.75,2)	1 (0.75,3)	-0316	0.752
Liver disorder	2 (1,3)	2 (1,2.25)	-0833	0.405
Cardiovascular disorder	4 (3.75,4)	4 (3,4)	-0.940	0.347
Central nervous system disorder	2 (1,3)	2 (1.75,3)	-1.969	0.051
Renal disorder	2 (2,3)	2 (2,3)	-0.030	0.976
APACHE II	23 (22,26)	28 (24.8,30.0)	-4.292	< 0.001
MPI	23.7 ± 5.4	27.4 ± 5.3	-3.051	0.003
Time to start enteral nutrition, days, median (IQR)	5 (3,6)	7 (5,10)	-3.290	0.001
CRRT, n (%)	29 (35.4)	7 (26.9)	0.633	0.292
Laparotomy, n (%)	80 (97.6)	25 (96.2)	0.145	0.704

APACHE II Acute Physiology and Chronic Health Evaluation II, CRP C-reactive protein, CRRT Continuous renal replacement therapy, CT Computed tomography, IQR Interquartile range, M ± SD Mean ± standard deviation, MPI Mannheim Peritonitis Index, PCT Procalcitonin, SIAI Severe intra-abdominal infection, SOFA Sequential organ failure assessment

Table 3.

Hospital course comparisons between survival and death group in SIAI patients due to gastrointestinal perforation

Hospital course	Survival group (n = 82)	Death group (n = 26)	Ζ	p
Mechanical ventilation duration, hours, median (IQR)	183 (97,240.25)	185 (90,264)	-0.273	0.785
ICU hospitalization time, hours, median (IQR)	264 (205.5,430)	264 (189,384)	-0.604	0.546
Length of hospital survival time, hours, median (IQR)	480 (296,726)	360 (260.5,521)	-1.521	0.128

ICU Intensive care unit, IQR Interquartile range, SIAI Severe intra-abdominal infection

Based on these results, a logistic regression analysis was conducted on variables associated with 28-day mortality in patients with SIAI due to gastrointestinal perforation (Fig. 3). The results indicated that low serum prealbumin level, infection from the stomach and duodenum versus other sites, and fungal infection were independent risk factors for increased 28-day mortality, whereas empirical use of antifungal drugs showed possible benefit to these patients.

Fig. 3.

Logistic regression analysis of variables associated with 28-day mortality in patients with severe intra-abdominal infection due to gastrointestinal perforation. APACHE II, Acute Physiology and Chronic Health Evaluation II; MPI, Mannheim Peritonitis Index; OR, odds ratio; PCT, procalcitonin

As demonstrated in Fig. 4, the primary target of anti-fungal agents was directed towards Candida. The 28-day mortality rate of empirical anti-fungal treatment was 2 (22.2%) and the 180-day survival rate was 14 (93.3%). Furthermore, the utilization of triazole antifungal medications was predominant (18, 94.7%).

Fig. 4.

Stacked bar chart comparing empirical antifungal therapy and targeted antifungal therapy groups, and a pie chart of fungal pathogen distributions

Characteristics associated with 180-day survival

As shown in Fig. 5A, the survival rate of the SIAI patients with stomach and duodenum perforation was significantly lower than that of the other site perforations. The Log-Rank test indicated a significant overall difference (p = 0.009), with median survival period of 111 days (stomach and duodenum), 177 days (colon and rectum), or 179 days (jejunum, ileum, and cecum). As shown in Fig. 5B, the survival rate of the mixed infection group was significantly lower than that of the single infection group. The Log-Rank test indicated a significant overall difference (p = 0.027), with an HR of 1.810 (1.069–3.065) and median survival period of 111 days (mixed infection) or 175 days (single infection).

Fig. 5.

Kaplan-Meier survival curves comparing overall survival among patients stratified by infection source (A) and infectious pathogen status (B)

Based on our results from Tables 1, 2 and 3, clinical practice, and expert advice, a COX regression analysis was conducted to identify the prognostic factors for 180-day survival in SIAI patients due to gastrointestinal perforation. The resultant forest plot (Fig. 6) indicated that diabetes (p = 0.047), malignant tumors (p = 0.016), initial serum albumin level below 30 g/L, prealbumin level below 300 mg/L, infection source control time exceeding 12 h (p < 0.001), and enteral nutrition initiation time exceeding 6 days (p = 0.001) were independent risk factors for the 180-day survival status of these patients. In contrast, patients with jejunum, ileum, cecum, or colon perforations had a better 180-day survival status than those with stomach or duodenum perforation.

Fig. 6.

Cox regression forest plot illustrating variables associated with 180-day survival in patients with severe intra-abdominal infection due to gastrointestinal perforation. APACHE II, Acute Physiology and Chronic Health Evaluation II; MPI, Mannheim Peritonitis Index

Discussion

Gastrointestinal perforation is an acute abdominal emergency, with an annual incidence of approximately one in 10,000 [15]. The condition is characterized by damage to the full thickness of the gastrointestinal wall, allowing the contents of the gastrointestinal tract to directly invade the sterile abdominal cavity. Without prompt and effective treatment, it can rapidly progress to SIAI, with a high mortality rate [16]. In the current study, the 28-day mortality rate of patients with SIAI due to gastrointestinal perforation was 24.1%, and the survival rate after six months of follow-up was 59.3%, suggesting that SIAI due to gastrointestinal perforation poses a significant mortality threat [17]. When evaluating factors for poor prognosis, in addition to well-established factors such as APACHE II and MPI scores [18–20], we have identified multiple other factors associated with a high 28-day mortality and low 180-day survival in SIAI patients with gastrointestinal perforation.

Protective biological substances, such as mucus and sodium bicarbonate, secreted by the gastrointestinal tract, decrease with age, leading to a decline in the defensive ability of the GI wall. When combined with multiple common comorbidities, elderly patients have an increased risk for developing gastrointestinal perforation [21]. Our study found a marginally significantly increased age in the death group versus the survival group (p = 0.053). We also found strong associations between 28-day mortality and smoking history, diabetes, cardiovascular disease, rheumatism, immune disorders, and a history of malignant tumors (p < 0.05). Multivariate logistic regression and COX survival analysis demonstrated that diabetes was an independent risk factor for adverse outcome in these patients (p = 0.047, HR = 2.094, 95% CI 1.009–4.344). Diabetic patients might be more prone to co-infection with Helicobacter pylori, a microbe closely associated with gastrointestinal perforation [22, 23]. Furthermore, hyperglycemia can exacerbate infection and make it more challenging to control, resulting in delayed organ repair, obstructed rehabilitation processes, and a poor prognosis [24]. Consequently, it is imperative to precisely regulate blood sugar to enhance the prognosis of these patients.

In this analysis, gastrointestinal perforation more frequently occurred in the stomach and duodenum than in the small intestine [25, 26]. However, the mortality rate was higher in colonic perforations (~ 45%) than stomach and duodenum perforations (~ 28%) [27, 28]. This might be explained by the fact that colonic perforation is often small and concealed, with patients frequently exhibiting atypical symptoms, leading to delayed clinical diagnosis and management [29]. However, our study only found that perforation of the stomach and duodenum was an independent risk factor for 28-day mortality and poor survival. The underlying mechanism might include the following three distinct aspects: (1) the patients included in this study were all severe cases with SIAI and multiple organ dysfunction, which was significantly different from the population in previous studies. (2) Different pathogenic characteristics occured in different gastrointestinal segments. Although bacterial load increases from the stomach to the colon [9, 30], the stomach and duodenal segment is rich in oxygen. Fungi are more tolerant of low pH environments and Gram-positive bacteria have virulence factors such as capsular polysaccharides, exotoxins, and adhesins. All of these may lead to a high chance of infection from Gram-positive bacteria and/or fungi following perforations at this site, thereby affecting prognosis [31–33]. (3) Disease composition bias might occur. Small intestinal perforation including appendiceal perforation can have a relatively low fatality rate, which may dilute the overall mortality risk of perforation at this site [34, 35], although no cases of appendiceal perforation were observed in our study. In conclusion, the poorer prognosis of perforation in the stomach and duodenum in patients with SIAI was the result of multiple factors, which merits particular consideration during clinical diagnosis and treatment.

Infection source control and antibiotic treatment are crucial considerations for management of SIAI from gastrointestinal perforation [36–39]. Our study demonstrated that an excess of 12 h of source control was an independent risk factor for unfavorable prognoses, which was consistent with the results of a meta-analysis from Song et al. [40]. Conservative drainage was effective in patients with abdominal cavity infection. Laparotomy did not impact prognosis.

Although controversial, most studies have shown that early anti-fungal treatment was associated with a reduced mortality in patients with gastrointestinal perforation [41–45]. Our study found that fungal infection resulted in a suboptimal prognosis, and empirical antifungal treatment was associated with decreased 28-day mortality rate (p = 0.020, HR = 1.009, 95% CI − 0.971–17.198). Most fungal infections (92.9%) are caused by Candida. Empirical antifungal treatment was primarily with azoles, and then targeted antifungal treatment, mainly with echinocandins. Therefore, we suggest that early and timely empirical antifungal therapy for SIAI patients with gastrointestinal perforation [18, 46, 47], although more prospective clinical trials should be performed on this treatment approach.

Nutritional status is one of the key factors affecting prognosis in patients with serious illnesses. Our study found that low serum albumin and low serum prealbumin were independent risk factors for patient prognosis, with was consistent with a previous meta-analysis showing that for every 10 g/L decrease in serum albumin, mortality rate increased by 137% [48]. The underlying mechanisms may involve increased catabolic stress, inadequate synthetic substrates, and further damage to intestinal barrier functions, leading to significantly worsened patient prognosis. Early, reasonable, and effective nutritional support can have a pivotal role in the improvement of the prognosis of patients suffering from SIAI due to gastrointestinal perforation [49]. This could be achieved through immune function regulation, accelerated repair of the intestinal mucosal barrier, and the promotion of organ function recovery [50].

This study found that, although early enteral nutrition therapy did not significantly reduce the 28-day mortality rate, it could significantly improve the 180-day survival of patients (p = 0.001, HR = 2.387, 95% CI − 1.414–4.029). This result should be viewed with caution, as the delayed initiation of enteral nutrition itself also indicated a more severe condition. The initiation of nutritional support in a timely manner has been demonstrated to be an effective strategy for reducing clinical complications, shortening hospital stays, and lowering medical costs [51]. However, patients with SIAI might have increased susceptibility to pathological changes, including intestinal wall edema, significant weakening of peristalsis, exacerbation of intestinal paralysis, and an abnormal increase in intestinal mucosal barrier permeability. Additionally, patients with gastrointestinal perforation might not be able to tolerate oral intake and enteral nutrition. In such critical situations, parenteral nutrition becomes a key alternative approach to maintaining nutritional status [52–54]. In terms of timing, a randomized controlled trial has demonstrated that the initiation time point of parenteral nutrition itself had no significant impact on patient survival rates [55]. The European Society for Clinical Nutrition and Metabolism guidelines propose that parenteral nutrition supplementation should be initiated within 48 h of the commencement of enteral nutrition (2–3 times/day) in cases where energy and protein intake remain below target levels [56]. Another study also suggested that, irrespective of patient baseline nutritional risk, if the actual energy supply from enteral nutrition continuously remains below 60% of the target calories, parenteral nutrition should be considered after one week to balance nutritional supply and metabolic load [57]. In clinical decision-making, a comprehensive evaluation of patient condition is imperative towards the balance between patient nutritional requirements and tolerance to nutrition supplies [58, 59]. Strategies should be adopted that can focus on early enteral nutrition, ensure precise assessment of needs, and facilitate dynamic adjustment of nutritional interventions. In the clinical diagnosis and treatment process, dynamic monitoring of PCT levels, comprehensive assessment of nutritional status, and combination with multi-dimensional scoring tools should be carried out to more accurately identify high-risk patients and facilitate prompt intervention strategies [60].

The present study had the following limitations. First, the retrospective study design, single-center research, and small sample size could bring information and selection bias into our study, restricting the generalizability of our study results. Second, the classification of infection sources is overly broad, lacking details on perforations in specific gastrointestinal segments whose distinct microbiota and anatomical features might influence patient disease severity and prognosis. Third, though we were able to obtain information on antibiotic and anti-fungi agent usage, we were unable to retrieve key data on the timing of initiating antibiotics, dosage, and treatment duration. All of these could certainly impact patient treatment responses and prognosis [61]. Furthermore, the risk of concomitant infection with drug-resistant bacteria has not been thoroughly evaluated [39]. Future prospective multi-center studies with large sample sizes should be performed to confirm our research findings.

Conclusions

SIAI patients due to gastrointestinal perforation could have a poor prognosis. The risk factors for a high mortality mainly included diabetes, underlying malignant tumors, and hypoproteinemia in these patients. Timely control of the infection source (within 12 h) and early initiation of enteral nutrition were key measures found to improve prognosis. Early and timely empirical antifungal treatment in addition to other necessary interventions might be considered in these patients.

Abbreviations

IAI

Intra-abdominal infection

SIAI

Severe intra-abdominal infection

BMI

Body mass index

PLT

Platelet

N%

Neutrophil ratio

PCT

Procalcitonin

CRP

C-reactive protein

APACHE II

Acute Physiology and Chronic Health Evaluation

SOFA

Sequential Organ Failure Assessment

MPI

Mannheim Peritonitis Index

Authors’ contributions

**Zhou Ye, Jiang Jin-Hua , Chen Yu-Ting** : Writing e review & editing, Writing e original draft, Visualization, Validation, Supervision, Software, Resources, Project administration, Methodology, Investigation, Formal analysis, Data curation, Conceptualization.

Funding

Joint Funds For The Innovation Of Science And Technology Of Fujian Province. 2025Y9190.

Data availability

The datasets generated and/or analysed during the current study are not publicly available due but are available from the corresponding author on reasonable request.

Declarations

Ethics approval and consent to participate

The study was approved by the Medical Ethics Committee of the First Affiliated Hospital of Fujian Medical University[approval number 2025 − 391]. All procedures performed in studies involving human participants were conducted in accordance with the ethical standards of the institutional and national research committees, as well as the 1964 Declaration of Helsinki and its subsequent amendments or comparable ethical standards. All patients provided informed consent, which were registered in the medical record.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.