INTRODUCTION

Sepsis and septic shock remain major causes of death in critically ill patients, especially when they progress to multiple organ dysfunction [1]. Infections caused by extended-spectrum beta-lactamase (ESBL)-producing Escherichia coli are particularly challenging because antimicrobial resistance may delay effective treatment and worsen outcomes [2]. The gastrointestinal tract is increasingly recognized as a key amplifier of systemic inflammation in critical illness through barrier disruption, altered host–microbiome interactions, and bacterial translocation [3,4].

These mechanisms may be especially relevant in patients with chronic intestinal disease, severe malnutrition, renal dysfunction, or recent immunosuppressive exposure [5]. In parallel, some patients with severe sepsis develop immune-metabolic features resembling persistent inflammation, immunosuppression, and catabolic syndrome, including lymphopenia, ongoing catabolism, and failure of biomarker recovery [6,7]. We report a fatal case of septic shock caused by ESBL-producing E. coli in a malnourished young adult with chronic enteropathy, marked gastrointestinal involvement, and a PICS-like trajectory during ongoing ICU deterioration despite organ support.

CASE REPORT

A 29-year-old man presented to the emergency department of a tertiary care hospital in Jakarta, Indonesia, in 2024 with a 2-day history of fatigue, watery diarrhea, vomiting, oliguria, dysuria, and scleral icterus. He also reported a 3-month history of chronic diarrhea and marked weight loss. His medical history was notable for intestinal tuberculosis and inflammatory bowel disease diagnosed 5 years earlier, and nephrotic syndrome treated 1 month before admission with diuretics and methylprednisolone use.

On admission, the patient appeared critically ill. Laboratory investigations showed a white blood cell count of 21.5 × 10⁹/L, an absolute lymphocyte count of 0.751 × 10⁹/L, a neutrophil-to-lymphocyte ratio of 25.9, creatinine of 326 µmol/L, sodium of 120 mmol/L, albumin of 12.1 g/L, and procalcitonin >32 µg/L. He was started on intravenous fluids, nutritional support, ceftriaxone, and metronidazole and was admitted to the ward. During the first hospital day, diarrhea worsened, melena developed, and oliguria persisted. Colonoscopy was planned to evaluate persistent diarrhea and gastrointestinal bleeding, but was deferred because of hemodynamic and neurological deterioration. On hospital days 3–4, he developed somnolence, worsening encephalopathy, and hypotension requiring intubation. He was transferred to the intensive care unit (ICU) on hospital day 5 because of progressive multiorgan dysfunction. A summary of the clinical course is shown in Table 1.

Table 1. Clinical timeline.

At ICU admission, repeat laboratory evaluation showed a hemoglobin level of 81 g/L, white blood cell count of 16.2 × 10⁹/L, creatinine level of 527 µmol/L, sodium level of 120 mmol/L, albumin level of 12.1 g/L, and procalcitonin level >32 µg/L. Non-contrast head computed tomography (CT) revealed no acute intracranial hemorrhage, territorial infarction, or mass effect (Figure 1A). Abdominal ultrasonography revealed cystitis, bilateral grade 2 renal parenchymal disease, and mild ascites. Within 9 h of ICU admission, the patient developed three seizures, which were treated with intravenous phenytoin and diazepam. He subsequently became hypotensive and required norepinephrine at a dose of up to 1.2 µg/kg/min. On ICU day 2, his condition worsened with upper gastrointestinal bleeding through the nasogastric tube, coagulopathy, severe metabolic acidosis, vasopressor-dependent shock, and anuric renal failure. Continuous venovenous hemodiafiltration was initiated. Blood cultures later grew extended-spectrum beta-lactamase (ESBL)-producing Escherichia coli, and the antimicrobial therapy was escalated accordingly. From ICU days 3 to 8, the patient remained critically ill, with recurrent seizures, abdominal distension, profuse diarrhea, persistent anuria, and ongoing organ support. Tracheostomy was performed on ICU day 6. Temporary hemodynamic improvement was observed during renal replacement therapy; however, it was not sustained. Daily ICU events and selected immune-inflammatory and metabolic trends are summarized in Table 2. Expanded day-by-day organ support and laboratory data are provided in Supplementary Tables S1A and S1B.

On ICU day 9, a repeat head CT demonstrated a new hypodense lesion in the posterior horn of the left lateral ventricle, with infarction included in the differential diagnosis (Figure 1B). Contrast-enhanced abdominal CT revealed diffuse bowel wall thickening involving the colon and small bowel without a definite focal source (Figure 2). On ICU day 10, the patient had refractory vasopressor-dependent shock, persistent anuria, severe hyperlactatemia, leukopenia, and worsening lymphopenia. Despite mechanical ventilation, vasopressors, renal support, broad-spectrum antimicrobials, and full resuscitative measures, the patient died on ICU day 10.

Figure 1. Serial non-contrast head CT at ICU admission and on day 9. (A) No acute intracranial abnormalities were observed at admission. (B) New hypodense lesion in the posterior horn of the left lateral ventricle on day 9, possibly indicating infarction.

Figure 2. Abdominal contrast-enhanced CT on ICU day 9 showing diffuse colonic and small bowel wall thickening without a definite focal source.

Table 2. Daily ICU events and selected immune-inflammatory and metabolic trends

Nota: ALC, absolute lymphocyte count; CRP, C-reactive protein; CT, computed tomography; CVVHDF, continuous venovenous haemodiafiltration; ESBL, extended-spectrum beta-lactamase; GI, gastrointestinal; HD, hemodialysis; ICU, intensive care unit; NLR, neutrophil-to-lymphocyte ratio; PCT, procalcitonin; RRT, renal replacement therapy; SCUF, slow continuous ultrafiltration.

Table S1A. Expanded day-by-day intensive care unit clinical and organ-support dataset

Table S1A (continued 1)

Note: ICU day 1 urine output was recorded over the first 14 hours after ICU admission. CRRT = continuous renal replacement therapy; CSF = cerebrospinal fluid; CT = computed tomography; CVVHDF = continuous venovenous haemodiafiltration; FiO₂ = fraction of inspired oxygen; HD = hemodialysis; MV = mechanical ventilation; NE = norepinephrine; PEEP = positive end-expiratory pressure; PS = pressure support; RR = respiratory rate; RRT = renal replacement therapy; SCUF = slow continuous ultrafiltration; SIMV = synchronized intermittent mandatory ventilation; TV = tidal volume; UF = ultrafiltration; UOP = urine output; VP = vasopressin.

Table S1B. Expanded day-by-day intensive care unit laboratory trends.

Note: On ICU day 2, the international normalized ratio was reported as >5 together with a prothrombin time >90 seconds. Albumin levels on ICU day 10 were not available in the daily laboratory summary. ALC, absolute lymphocyte count; CRP, C-reactive protein; Hb, hemoglobin; NLR, neutrophil-to-lymphocyte ratio; PCT, procalcitonin; PT, prothrombin time; WBC, white blood cell count.

DISCUSSION

This case illustrates rapidly progressive septic shock with refractory multiorgan failure in a patient with gastrointestinal vulnerability. Chronic enteropathy, prior intestinal tuberculosis, severe malnutrition, nephrotic syndrome with renal involvement, recent methylprednisolone exposure, and profound hypoalbuminemia likely reduced gastrointestinal, renal, immune, and metabolic reserves before the onset of bloodstream infection. The course progressed from organ dysfunction at presentation to vasopressor-dependent shock, anuric acute kidney injury requiring renal replacement therapy, coagulopathy with bleeding, encephalopathy, recurrent seizures, and death on ICU day 10. This trajectory is consistent with the high mortality associated with septic shock complicated by multiple organ dysfunction [1]. Bloodstream infection caused by ESBL-producing Escherichia coli remains clinically significant because antimicrobial resistance may delay appropriate therapy and worsen outcomes [2]. Severe malnutrition and persistent hypoalbuminemia may have weakened host defence and physiological reserve [5].

A central feature of this case was the gastrointestinal signal. Chronic watery diarrhea, gastrointestinal bleeding, abdominal distension, bilious nasogastric drainage, and diffuse bowel wall thickening on contrast-enhanced abdominal CT suggested intestinal involvement. The gut is increasingly recognized as an amplifier of systemic inflammation in critical illness through barrier disruption, altered host–microbiome interactions, local immune dysregulation, and bacterial or bacterial product translocation [8,9]. In this patient, chronic enteropathy, prior intestinal tuberculosis, and severe malnutrition may have compromised mucosal integrity. However, the source of the infection could not be definitively established. A gastrointestinal source remained biologically plausible, but a urogenital source also remained possible because dysuria, urinalysis abnormalities, and suspected cystitis were present. The most defensible interpretation was septic shock with gastrointestinal involvement and unresolved source localization rather than proven primary intra-abdominal sepsis. Another aspect was the longitudinal immune-metabolic pattern. The absolute lymphocyte count declined from 0.751 × 10⁹/L at presentation to 0.334 × 10⁹/L in the terminal phase, profound hypoalbuminemia persisted, and lactate levels increased to 10.5 mmol/L during refractory shock. The decline in neutrophil-to-lymphocyte ratio did not indicate recovery, because it occurred in the context of severe leukopenia and worsening lymphopenia rather than physiological improvement. Serial changes in lymphocyte count, neutrophil-to-lymphocyte ratio, and lactate have been associated with prognosis in sepsis [10,11]. Taken together, persistent hypoalbuminemia, progressive lymphopenia, rising lactate levels, and failure of biomarker recovery support an immune-metabolic failure pattern with a PICS-like trajectory, although the short clinical course precludes a definitive diagnosis of PICS [7]. Neurological deterioration was likely multifactorial, and the encephalopathy, recurrent seizures, and hypodense lesion on repeat head CT may reflect mechanisms described in sepsis-associated encephalopathy [12].

From a therapeutic perspective, this case highlights empiric antibiotic selection in source-uncertain septic shock [13]. Given the severity of the illness, acute kidney injury, and subsequent confirmation of ESBL-producing E. coli bacteremia, early broad-spectrum gram-negative coverage may have been more appropriate in a high-risk patient with multidrug-resistant infection [14]. Anuric renal failure requiring continuous venovenous haemodiafiltration, slow continuous ultrafiltration, and hemodialysis underscores the importance of PK/PD-guided antimicrobial dose optimization during critical illness [15]. This case shows how host vulnerability, source uncertainty, resistant gram-negative bacteremia, progressive immune-metabolic deterioration, and organ-support complexity can converge in fulminant septic shock, leading to refractory decline despite antimicrobial escalation and maximal ICU support.

CONCLUSION

This case highlights immune-metabolic failure in septic shock caused by ESBL-producing Escherichia coli with gastrointestinal involvement. Hypoalbuminemia, lymphopenia, rising lactate levels, and absent biomarker recovery supported a PICS-like trajectory. Serial biomarkers may identify high-risk deterioration, supporting source reassessment and antimicrobial optimization.

DECLARATIONS

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CONSENT FOR PUBLICATION

The Authors agree to the publication in the Journal of Society Medicine.

FUNDING

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COMPETING INTERESTS

All authors have reviewed and approved the final version of the manuscript and agreed to its publication in the Journal of Society Medicine.

AUTHORS’ CONTRIBUTIONS

L.S.P. contributed to the conception and design of the case report, acquisition and interpretation of clinical data, visualization, and drafting of the manuscript. V.I. contributed to the supervision, critical revision of the manuscript for important intellectual content and manuscript refinement. All authors have read and approved the final manuscript and have agreed to be accountable for all aspects of the work.

ACKNOWLEDGMENTS

The authors acknowledge all healthcare professionals who contributed to the care and management of the patient.

REFERENCE