INTRODUCTION

Intra-abdominal infections (IAIs) are a significant cause of sepsis and septic shock, posing a critical challenge to surgeons, intensivists, and related disciplines worldwide [1]. Despite advancements in preventive measures, such as adherence to the Joint Commission International accreditation standards, sepsis management aligned with the Surviving Sepsis Campaign (SSC) guidelines, and rational antibiotic use, IAIs continue to be a persistent issue in Indonesia [1–4].

Global mortality rates for abdominal sepsis range from 3% to 42%, reflecting the severity and variability of outcomes [5]. In Indonesia, data from six major hospitals indicate that the primary sources of IAIs include appendicitis (26.64%), gastric and duodenal ulcers (22.70%), small intestine (11.84%), large intestine (13.16%), postoperative complications (9.54%), and other causes (16.12%) [5]. Microbiological cultures commonly identify Escherichia coli (35.41%), Klebsiella pneumoniae (13.44%), Enterobacter cloacae (9.34%), Proteus mirabilis (8.69%), and Enterococcus faecalis (7.87%) as predominant pathogens [5]. Intra-abdominal sepsis originates from infections within the abdominal cavity, often leading to diffuse or localized peritonitis [6]. The gastrointestinal tract, frequently described as the "motor of sepsis," harbors a high bacterial load, underscoring the need for early diagnosis to prevent progression to severe sepsis or septic shock [6]. Complications such as acute respiratory distress syndrome (ARDS), characterized by acute-onset respiratory failure within seven days of an insult, bilateral opacities on chest X-ray, and hypoxemia not attributed to cardiac failure, further elevate mortality risk [7]. ARDS management often necessitates mechanical ventilation with a lung-protective strategy to mitigate hypoxemia [7]. Delayed diagnosis and inadequate source control significantly increase mortality, emphasizing the importance of prompt surgical intervention and aggressive management [6].

Effective management of IAI with septic shock and ARDS in the intensive care unit (ICU) requires a multifaceted approach, including fluid and nutritional support, analgesia, sedation, thrombosis prophylaxis, glycemic control, prevention of stress ulcers, and targeted antibiotic therapy [6]. Additionally, strategies to minimize ventilator-associated complications, such as ventilator-associated pneumonia (VAP), are critical to improving outcomes [6]. This case report examines the diagnosis and management of a patient with intra-abdominal infection complicated by septic shock and ARDS in the ICU, highlighting evidence-based strategies to optimize clinical outcomes.

CASE DESCRIPTION

A 59-year-old male patient, identified as Mr. T (medical record number: 0002124648), with a body weight of 65 kg and height of 160 cm, presented to the emergency department with a five-day history of diffuse abdominal pain, fever for three days, and inability to defecate or pass flatus for two days. On arrival, the patient appeared lethargic and apathetic, with vital signs indicating septic shock: blood pressure of 76/46 mmHg, heart rate of 146 beats per minute, respiratory rate of 28 breaths per minute, and oxygen saturation of 97% on a non-rebreather mask at 10 liters per minute. Physical examination revealed anemic conjunctivae, non-icteric sclerae, vesicular breath sounds bilaterally without adventitious sounds, and regular heart sounds without murmurs. Abdominal examination demonstrated distension, decreased bowel sounds, and diffuse tenderness. The liver and spleen were not palpable due to distension. An indwelling urinary catheter was placed, yielding 100 mL of turbid, yellow urine.

Laboratory findings on admission showed haemoglobin of 9.8 g/dL, leukocytosis (26,000/µL), thrombocytopenia (357,000/µL), hyponatraemia (132 mEq/L), normal potassium (3.6 mEq/L), chloride (105 mEq/L), hypocalcaemia (4.93 mg/dL), magnesium (1.9 mg/dL), elevated urea (131.8 mg/dL), creatinine (2.51 mg/dL), normal liver enzymes (SGOT 39 U/L, SGPT 39 U/L), prothrombin time (PT) of 15 s, activated partial thromboplastin time (APTT) of 28.4 s, INR of 1.06, hypoalbuminaemia (2.8 g/dL), and elevated lactate (4.7 mmol/L). Arterial blood gas analysis revealed a pH of 7.34, pO2 of 148.7 mmHg, pCO2 of 24.5 mmHg, base excess of -8.5 mmol/L, HCO3 of 14.6 mmol/L, and a P/F ratio of 341, which was consistent with metabolic acidosis. Chest radiography revealed cardiomegaly but no pulmonary abnormalities. The patient was diagnosed with septic shock secondary to generalised peritonitis caused by incarceration of the hernia.

Initial management included aggressive fluid resuscitation with 1,500 mL of Ringer’s lactate over one hour and norepinephrine titration to achieve a mean arterial pressure (MAP) greater than 65 mmHg. An emergency exploratory laparotomy was performed, which revealed 300 mL of purulent peritoneal fluid. Intraoperative fluid management consisted of 1,000 mL of Ringer’s lactate, with an estimated blood loss of 200 mL and a urine output of 150 mL over a four-hour procedure. Postoperatively, the patient was admitted to the intensive care unit (ICU) and placed on mechanical ventilation. Antibiotic therapy was initiated with meropenem (1 g every 8 h) and metronidazole (500 mg every 8 h) intravenously. Fluid management included 1,500 mL of intravenous fluid per 24 h. Analgesia was provided with fentanyl 0.5 mcg/kg/hour and paracetamol 1 g every 8 hours, and the patient was kept nil per os (NPO). Sedation was managed with midazolam (3 mg/h), which was transitioned to dexmedetomidine on day four. Omeprazole (40 mg daily) was administered for gastric prophylaxis, but thromboprophylaxis was withheld during the ICU stay.

The patient’s fluid balance was closely monitored (Table 1). On day one, the total fluid input was 5,636 mL (infusion: 5,000 mL, medications: 500 mL, transfusion: 636 mL), with an output of 2,849 mL (urine: 440 mL, nasogastric tube: 300 mL, drain: 500 mL, blood loss: 500 mL, insensible losses: 600 mL), resulting in a positive balance of 2,787 mL. By day six, the cumulative fluid balance was negative (-118 mL), reflecting improved renal function and diuresis. Laboratory trends (Table 2) showed initial anaemia (haemoglobin 7.8 g/dL on day one, improving to 9.6 g/dL by day six), resolving leukocytosis (13,200/µL on day one to 20,300/µL on day six), and improving renal function (creatinine 0.96 mg/dL on day one to 0.56 mg/dL by day five). Procalcitonin levels decreased from 10.62 ng/mL on day two to 0.52 ng/mL by day seven, indicating resolution of infection. No microbiological cultures were obtained during hospitalisation.

On day four, norepinephrine was discontinued as haemodynamic stability was achieved. The patient was extubated on day five and transitioned to enteral feeding with Peptamen, starting at 50 mL every four hours on day three and increasing to 100 mL every four hours on day four. The patient was transferred to the high-care unit on day six, demonstrating significant clinical improvement. This case highlights the critical role of timely surgical intervention, targeted antimicrobial therapy, and comprehensive ICU management in achieving favourable outcomes in patients with septic shock secondary to intra-abdominal infection.

Table 1. Fluid Balance During ICU Stay

Noted: Total fluid input includes infusion, drugs, transfusion, and diet. Total fluid output includes urine, nasogastric tube (NGT), drain, bleeding, and insensible water loss (IWL).

Table 2. Laboratory Results During ICU Stay

Note: Procalcitonin levels: 10.62 ng/mL (day 2), 0.52 ng/mL (day 7)

DISCUSSION

Intra-abdominal infections (IAIs) complicated by septic shock represent a significant clinical challenge owing to their high morbidity and mortality, particularly in the intensive care unit (ICU) setting. In the present case, a 59-year-old man with generalised peritonitis secondary to an incarcerated hernia developed septic shock, necessitating urgent surgical intervention and comprehensive ICU management. The patient’s condition aligned with the classification of community-acquired complicated IAI, characterised by peritonitis due to hollow viscus perforation, as described by Sartelli et al. [2].

The intraoperative finding of 300 mL of purulent peritoneal fluid confirmed secondary peritonitis resulting from the migration of gastrointestinal flora into the peritoneal cavity following anatomical barrier disruption [8].The absence of microbiological cultures in this case, despite the recommendation by the Surviving Sepsis Campaign (SSC) to obtain cultures prior to antibiotic initiation, limited the ability to tailor therapy but did not preclude effective empirical treatment with meropenem and metronidazole [3]. This regimen is appropriate given the high prevalence of Escherichia coli and Klebsiella pneumoniae in complicated IAIs in Indonesia, as reported by Moenadjat et al.[5]

Timely diagnosis and management of IAI in this patient were critical for achieving a favourable outcome. The patient presented with classic clinical signs of peritonitis, including diffuse abdominal pain, distension, and muscular guarding, corroborated by leukocytosis (26,000/µL) and elevated lactate levels (2.7 mmol/L), indicative of acute infection and tissue hypoperfusion [9,10]. Although abdominal plain radiography confirmed pneumoperitoneum, suggesting hollow viscus perforation, the decision to proceed with exploratory laparotomy within 4.5 h of presentation was pivotal, aligning with guidelines emphasising early source control to reduce mortality [4,20]. Delays in surgical intervention for IAI are associated with increased mortality, with each hour of delay contributing to adverse outcomes [20]. Successful source control in this case, as evidenced by the evacuation of purulent fluid and management of the incarcerated hernia, underscores the importance of rapid surgical intervention in mitigating the inflammatory cascade driven by bacterial translocation and cytokine release, including tumour necrosis factor-α (TNF-α) and interleukins (IL-1, IL-6) [11].

Septic shock, diagnosed on day one based on the need for vasopressor support (norepinephrine 0.1 mcg/kg/min) and elevated lactate (4.6 mmol/L), reflects the systemic inflammatory response and endothelial dysfunction characteristic of abdominal sepsis [1,11]. The initial fluid resuscitation with 1,500 mL of Ringer’s lactate in the emergency department, equivalent to approximately 23 mL/kg, was slightly below the SSC-recommended 30 mL/kg for septic shock but was sufficient to stabilise haemodynamics in conjunction with norepinephrine [3]. The lack of serial lactate measurements to assess resuscitation adequacy, as recommended by the SSC 2021, represents a deviation from optimal practice, potentially limiting the ability to confirm the resolution of tissue hypoperfusion [3,16]. Fluid management transitioned to a negative balance by day four (-500 to -700 mL/24 h), consistent with deresusitation strategies to minimise complications, such as prolonged ventilation and acute kidney injury [24]. The patient’s improving renal function (creatinine decreased from 0.96 mg/dL to 0.56 mg/dL by day five) and decreasing procalcitonin levels (from 10.62 ng/mL on day two to 0.52 ng/mL on day seven) suggested effective infection control and haemodynamic stabilisation.

Antimicrobial therapy with meropenem and metronidazole was initiated empirically, targeting the polymicrobial nature of IAIs, particularly gram-negative and anaerobic pathogens prevalent in secondary peritonitis [2,5]. The 10-day duration of therapy aligns with SSC recommendations for short-course therapy (7–10 days) in the presence of adequate source control [2]. However, the absence of microbiological cultures precluded de-escalation to a narrower-spectrum regimen, a practice recommended to reduce antimicrobial resistance and optimize therapy [2,3]. The patient’s clinical improvement, evidenced by extubation on day five and transfer to the high-care unit on day six, supports the efficacy of the chosen regimen despite the lack of culture-guided therapy. The high-risk nature of this case, owing to delayed presentation and diffuse peritonitis, justified the use of broad-spectrum antibiotics, as outlined in the algorithm for extra-biliary IAI management [2].

Supportive care in the ICU adhered to the FASTHUG framework (Feeding, Analgesia, Sedation, Thromboembolic prophylaxis, Head-of-bed elevation, Ulcer prophylaxis, Glycaemic control), with some deviations from the protocol. Enteral nutrition was initiated on day three with Peptamen, progressing from 50 mL to 100 mL every four hours, which was delayed compared to the American Society for Parenteral and Enteral Nutrition (ASPEN) recommendation of starting within 24–48 hours for critically ill patients at high nutritional risk [25]. The patient’s low malnutrition risk (NRS 2002 <3) may have justified this delay, but earlier initiation could have optimised gut integrity and reduced infectious morbidity [25-37]. Analgesia and sedation with fentanyl, paracetamol, and dexmedetomidine (replacing midazolam on day four) achieved target scores on the Critical Care Pain Observation Tool (CPOT: 0–1) and Richmond Agitation-Sedation Scale (RASS: 0 to -2), aligning with guidelines to minimise benzodiazepine use and prevent delirium [28,29]. The omission of thromboprophylaxis, despite the patient’s low risk for venous thromboembolism (VTE) based on Padua/IMPROVE scores, was reasonable given the postoperative bleeding risk; however, daily VTE monitoring should have been emphasised [33–35]. Omeprazole (40 mg/day) for stress ulcer prophylaxis was appropriate given the patient’s risk factors (septic shock and mechanical ventilation), although long-term proton pump inhibitor use warrants caution due to the potential risk of Clostridium difficile infection [37].

CONCLUSION

Intra-abdominal infections with septic shock are a critical challenge in the ICU, associated with high morbidity and mortality. This case highlights the success of rapid diagnosis, timely surgical source control, early broad-spectrum antibiotics, and multidisciplinary ICU care in achieving favorable outcomes. Despite limitations such as absent microbiological cultures and delayed enteral nutrition, adherence to evidence-based protocols improved survival. Enhanced diagnostics and guideline compliance are essential for optimizing care in resource-limited settings.

DECLARATIONS

None

CONSENT FOR PUBLICATION

The Authors agree to be published in the Journal of Society Medicine.

FUNDING

None

COMPETING INTERESTS

The authors declare no conflicts of interest in this case report.

AUTHORS’ CONTRIBUTIONS

All authors made substantial contributions to the case report. DFN was responsible for patient management, data collection, and initial drafting of the manuscript. All authors reviewed and approved the final version of the manuscript, ensuring its accuracy and integrity, and are accountable for all aspects of the work.

ACKNOWLEDGMENTS

None

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