Published online Sep 26, 2026. doi: 10.12998/wjcc.126787
Revised: September 16, 2026
Accepted: October 10, 2026
Published online: September 26, 2026
Processing time: 61 Days and 19 Hours
Perforation is a rare but potentially fatal complication of upper gastrointestinal endoscopy, particularly when therapeutic maneuvers are performed. Posterior gastric wall perforation is particularly difficult to recognize because it may deco
On emergency department admission, the patient presented with a blood pressure of 84/50 mmHg, metabolic acidosis, and anuria, suggesting septic shock. Serum creatinine had risen from a documented baseline of 1.1 mg/dL to 4.18 mg/dL, corresponding to Kidney Disease: Improving Global Outcomes stage 3 acute kidney injury (AKI). Contrast-enhanced abdominal computed tomography demonstrated discontinuity of the posterior wall of the gastric corpus, with extravasation of contrast material into the retrogastric space and lesser sac, together with widespread free intraperitoneal air and fluid. AKI was considered predominantly sepsis-associated ischemic acute tubular injury (ATI); contrast exposure seven days earlier was regarded as a possible but unproven contributory factor. The patient underwent two surgical interventions—gastric wedge resection with feeding jejunostomy and re-laparotomy with small bowel resection, double-barrel ileostomy, and surgical gastrostomy due to a jejunostomy-related bile leak. Despite maximal intensive care unit support, the patient died on the 16th day of admission.
Posterior gastric perforation may present with minimal peritoneal signs in patients with altered anatomy and impaired communication, and AKI in this setting is usually multifactorial, dominated by sepsis-associated ischemic ATI.
Core Tip: Posterior gastric wall perforation is a rare, easily missed complication of upper gastrointestinal endoscopy because it may decompress into the lesser sac rather than the peritoneal cavity. In this high-risk patient, the endoscope had to be advanced posterior to a migrated tracheoesophageal voice prosthesis during a session that also included esophageal bougie dilation, while thoracolumbar scoliosis, pectus carinatum, and nonverbal status masked peritonitis for 72 hours. The accompanying acute kidney injury (AKI) was multifactorial, most consistent with sepsis-associated ischemic acute tubular injury rather than contrast-associated AKI. Early cross-sectional imaging may be warranted when high-risk patients deteriorate after endoscopy.
- Citation: Cakiroglu OF, Gurbuz J, Taslidere B, Cander B. Posterior gastric wall perforation and acute kidney injury after upper endoscopy with esophageal dilation: A case report. World J Clin Cases 2026; 14(27): 126787
- URL: https://www.wjgnet.com/2307-8960/full/v14/i27/126787.htm
- DOI: https://dx.doi.org/10.12998/wjcc.126787
Perforation during upper gastrointestinal endoscopy is a rare but potentially fatal complication, with an incidence reported between 0.03% and 0.1%[1,2]. Posterior gastric wall perforations are particularly uncommon and diagnostically challenging, as they may decompress into the lesser sac rather than the free peritoneal cavity, producing subtle or atypical peritoneal signs[3,4]. In patients with pre-existing anatomical deformities, communication barriers, or multiple comorbidities, the clinical picture may be further obscured, leading to delayed recognition and increased morbidity.
Upper gastrointestinal endoscopy is technically more demanding in patients whose upper aerodigestive anatomy has been substantially altered. Previous total laryngectomy and cervical radiotherapy modify the pharyngoesophageal inlet and reduce tissue compliance; an indwelling or migrated tracheoesophageal voice prosthesis may occupy part of the esophageal lumen and require the endoscopist to advance the instrument alongside a fixed foreign body; and severe thoracolumbar scoliosis with chest wall deformity distorts the axis of the esophagus and stomach, making a coaxial, tension-free scope position more difficult to maintain. In such patients, the mechanical forces transmitted to the gastric wall during routine advancement and insufflation are likely to be greater than usual, while the classical clinical signs that would normally indicate an injury are least reliable[5,6].
Acute kidney injury (AKI) in critically ill surgical patients is most commonly driven by hemodynamic compromise and sepsis-associated ischemic acute tubular injury (ATI). Contrast-associated AKI (CA-AKI)—the term now preferred over the older designation “contrast-induced nephropathy”—is a diagnosis of exclusion that requires concurrent and more prevalent etiologies to be considered first[7,8]. We present a case in which both mechanisms—surgical sepsis and prior contrast exposure—converged, compounding diagnostic and management complexity.
Reports that combine a delayed, endoscopy-associated posterior gastric perforation with a competing contrast-related explanation for concurrent AKI are scarce. The specific knowledge gap addressed by this case is therefore twofold: Which post-endoscopy features should prompt urgent cross-sectional imaging in a patient whose examination and history are unreliable, and how should competing causes of AKI be weighed when recent contrast exposure coincides with septic shock?
A 64-year-old male presented to the emergency department by ambulance after experiencing syncope.
Seven days before admission, contrast-enhanced computed tomography (CT) of the neck, thorax, and abdomen was performed for oncological surveillance; baseline creatinine at that time was 1.1 mg/dL [estimated glomerular filtration rate (eGFR), 62 mL/minute/1.73 m2], and no new pathology was identified. Three days before admission, upper gastrointestinal endoscopy was performed for feeding difficulty. The endoscopy report documented migration of the tracheoesophageal voice prosthesis into the esophageal lumen, requiring the endoscopist to advance the scope with resistance posterior to the device to reach the thoracic esophagus. During the same session, bougie dilation of a known iatrogenic stricture of the proximal esophagus was performed, and five gastric biopsies were obtained from the prepyloric region, antral posterior wall, greater curvature, incisura angularis, and lesser curvature; the greater- and lesser-curvature samples were registered by the pathology laboratory as antral, and no biopsy was labeled as having been taken from the gastric corpus. The esophagus, gastric fundus, corpus, and duodenum showed no ulceration, polyp, or mass; the antral mucosa was hyperemic and edematous. Prosthesis removal was recommended. No perforation or immediate complication was documented intraprocedurally. During the three days between endoscopy and admission, the patient remained at home; because he was unable to communicate verbally, no reliable symptom history for this interval could subsequently be obtained.
His medical history included hypertension, atrial fibrillation, hypothyroidism, prior stroke, advanced thoracolumbar scoliosis, laryngeal carcinoma treated with laryngectomy and radiotherapy in 2009, tracheoesophageal voice prosthesis placement in 2019, coronary angiography one year prior, and implantable cardioverter-defibrillator insertion two months prior. An earlier upper endoscopy, performed for epigastric pain, had documented an iatrogenic stricture of the proximal esophagus, pangastritis, and antral ulcer scars; biopsies had shown chronic active gastritis with Helicobacter pylori
A detailed personal and family history could not be obtained because the patient was unable to communicate verbally at presentation and the admission was an emergency. No family history of gastrointestinal or renal disease was reported by the accompanying relative, and family history was not considered contributory to the acute presentation.
On admission, blood pressure was 84/50 mmHg, heart rate 68 bpm, temperature 36.8 °C, and SpO2 88%. The patient communicated only by blinking. Abdominal examination revealed distension and guarding; rebound tenderness could not be reliably assessed because of scoliosis and pectus carinatum. A urinary catheter yielded no urine output.
Laboratory results showed creatinine 4.18 mg/dL (baseline 1.1 mg/dL), eGFR 14 mL/minute/1.73 m2, blood urea nitrogen (BUN) 103 mg/dL, C-reactive protein 359 mg/L, troponin I 273.2 ng/L, and potassium 6.56 mEq/L. Arterial blood gas analysis showed pH 7.19, HCO3- 18.4 mmol/L, and base excess -9.5 mmol/L, consistent with metabolic acidosis and partial respiratory compensation. The rise in serum creatinine to 3.8 times the documented baseline, together with anuria persisting beyond 12 hours, corresponded to stage 3 AKI according to the Kidney Disease: Improving Global Outcomes (KDIGO) classification[9]. Because the patient was anuric, no urine was available for urinalysis or urine microscopy at presentation. Troponin elevation was attributed to type 2 myocardial infarction secondary to hemody
Bedside echocardiography revealed no wall motion abnormalities and preserved systolic function. Contrast-enhanced abdominal CT demonstrated a focal discontinuity of the posterior wall of the gastric corpus, with extravasation of orally administered and intravenous contrast material into the retrogastric space and lesser sac, extensive free intraperitoneal air, and diffuse free fluid in all four quadrants. Marked thoracolumbar scoliosis with consequent distortion of the upper abdominal viscera was also evident. These findings were considered diagnostic of gastric perforation with generalized peritoneal contamination (Figure 1).
Histopathological examination: The gastric wedge resection specimen (7 cm × 2 cm × 1.5 cm, with a 7-cm staple line) contained a 2.5 cm × 2.2 cm serosal defect. Microscopy showed diffuse mucosal erosion, submucosal hemorrhage, and edema, with features of perforation, together with focal foveolar hyperplasia and chronic inflammation with glandular dilation. No chronic peptic ulcer, intestinal metaplasia, or neoplasia was reported. H. pylori was not identified on Giemsa staining, and immunohistochemical staining for p53 was negative. The biopsies obtained during the index endoscopy showed moderate-to-severe chronic active gastritis, with heavy H. pylori colonization and no atrophy or intestinal metaplasia in the prepyloric sample.
Posterior gastric wall perforation temporally associated with, and considered most likely related to, the preceding upper gastrointestinal endoscopy with esophageal bougie dilation and gastric biopsies, complicated by four-quadrant bile-stained peritonitis and septic shock. KDIGO stage 3 AKI, was considered predominantly sepsis-associated ischemic ATI, with CA-AKI from contrast exposure 7 days earlier regarded as a possible contributory factor. Type 2 myocardial infarction secondary to hemodynamic stress.
Following multidisciplinary consultation, emergency surgery was performed on the day of admission. Endoscopic or conservative management was not considered appropriate given the size of the defect, the 72-hour delay since the index procedure, and the presence of established four-quadrant peritoneal contamination; open surgical source control was therefore undertaken. Intraoperatively, four-quadrant bile-stained peritoneal contamination was found. The gastrocolic ligament was divided and the lesser sac explored, revealing a 2.5-cm full-thickness defect in the posterior wall of the gastric corpus along the greater curvature. The stomach was mobilized to the esophagogastric junction. Intraoperative endoscopy via the perforation site identified the voice prosthesis in its expected esophageal position. A 60-mm green Echelon stapler was used to perform gastric wedge resection of the perforated segment, and the staple line was reinforced with Vicryl sutures. A feeding jejunostomy was fashioned using the Witzel technique 40 cm distal to the ligament of Treitz, with enteral rather than parenteral access preferred because a prolonged period of gastric rest was anticipated. Four silicone drains were placed, and the specimen was sent for histopathological analysis.
Postoperatively, the patient was admitted to the intensive care unit (ICU). On ICU day 2, continuous veno-venous hemofiltration (CVVH) was initiated for refractory oliguria and azotemia. CVVH was continued until death, and renal function did not recover. CT performed during ICU follow-up revealed a left atrial thrombus (17 mm × 10 mm); bedside transthoracic echocardiography performed during the same period demonstrated an additional, anatomically distinct left ventricular apical thrombus, without wall motion abnormalities or systolic dysfunction. Two separate intracardiac thrombi were therefore documented in this patient: One in the left atrium on CT and one at the left ventricular apex on echocardiography. Cardiology initiated therapeutic low-molecular-weight heparin; a cardiovascular surgery consultation was obtained, and no urgent intervention was deemed necessary. A periportal fluid collection (63 mm × 34 mm) was also noted and monitored conservatively. Potassium normalized to 4.2 mEq/L with medical treatment.
On postoperative day 10, bile output was noted from the abdominal drains. Re-laparotomy revealed detachment of the jejunostomy catheter from the abdominal wall with resultant bile leakage into the peritoneal cavity; the gastric staple line was intact. The perforated jejunal segment was resected using an EndoGIA stapler, and a side-to-side jejunal anastomosis was constructed with an Echelon stapler and reinforced with Vicryl sutures. A drain-related pressure injury to an adjacent ileal loop, nearly causing secondary perforation, was identified; the affected segment was exteriorized as a double-barrel ileostomy through the right lower quadrant. A surgical gastrostomy was additionally performed via a Pezzer catheter through the gastric corpus, remote from the prior staple line, for enteral access. Three new silicone drains were placed, and the abdomen was closed. Histopathological examination of the resected 34-cm small-bowel segment showed a 1-cm perforation with full-thickness congestion and ulceration, deep fissuring tracts, reparative epithelial changes, and active serositis with fibrinous exudate; ischemic necrosis with ulceration was present at the surgical margins.
Supportive management included broad-spectrum antimicrobial therapy (meropenem, vancomycin, micafungin, tigecycline), vasopressor support, mechanical ventilation via tracheostomy (BiLevel mode, FiO2 70%-100%, PEEP 8
Despite maximal intensive care support, the patient’s condition continued to deteriorate. On April 30, 2025 (postoperative day 16, corresponding to hospital day 16 because the index operation was performed on the day of admission), the patient died in the ICU from refractory multiorgan failure with persistent vasopressor dependence, ongoing renal replacement therapy, and progressive respiratory failure despite source control and broad-spectrum antimicrobial coverage.
The 3-day interval between endoscopy and clinical presentation is consistent with a delayed posterior gastric perforation, a recognized—if uncommon—pattern. Unlike anterior perforations, posterior gastric wall defects may drain preferentially into the lesser sac, limiting early peritoneal contamination and attenuating classical signs of peritonitis[3,4]. The index procedure, however, was not purely diagnostic. The scope had to be advanced with resistance posterior to the migrated voice prosthesis to reach the thoracic esophagus, bougie dilation of an iatrogenic proximal esophageal stricture was performed, and five gastric biopsies were obtained. Therapeutic maneuvers, and dilation in particular, carry a higher risk of perforation than diagnostic examination[1,2]. None of these maneuvers, however, was directed at the site of the defect: Dilation was confined to the proximal esophagus, and the biopsies were taken from the prepyloric region, antrum, and incisura angularis rather than from the posterior wall of the corpus. A direct dilator- or biopsy-related injury at the perforation site therefore appears unlikely, although it cannot be excluded with certainty. A more plausible, but unproven, explanation is that a prolonged therapeutic session—with passage of the endoscope and dilators against resistance and the gastric insufflation needed to maintain the view—exposed a stomach already displaced by severe thoracolumbar scoliosis to increased mechanical and distension-related stress. Gastric perforation remote from the instrument tip has been attributed to excessive insufflation during upper endoscopy[10]. No perforation was recognized during the procedure, and no immediate post-procedural imaging was obtained; an iatrogenic mechanism is therefore probable on the basis of the temporal relationship and the exclusion of alternative pathology, but it is not definitively established.
Alternative etiologies were also considered. Because the patient had H. pylori-associated chronic active gastritis and previously documented antral ulcer scars, a perforated peptic ulcer had to be excluded. Histopathology of the perforation site, however, showed diffuse mucosal erosion with submucosal hemorrhage and edema, with no chronic ulcer; H. pylori was not identified in the resected specimen, no ischemic necrosis or neoplasia was described, and p53 immunostaining was negative. Use of nonsteroidal anti-inflammatory drugs or corticosteroids was not documented. These findings, together with the close temporal relationship to the procedure, support—but do not prove—an iatrogenic mechanism[5,11].
Published series of upper gastrointestinal endoscopic complications are dominated by esophageal and duodenal injuries, and gastric perforation is comparatively uncommon; when it occurs, it is usually recognized during or shortly after the procedure[1,2]. The present case differs in three respects: Recognition was delayed by 72 hours; the defect lay on the posterior wall of the corpus, remote from both the dilated esophageal segment and the biopsy sites; and it decompressed into the lesser sac. Gastric perforation remote from the site of instrumentation has been described after excessive insufflation; in the reported case, the tear involved the lesser curvature of the gastric body[10]. We are not aware of any series reporting the frequency of posterior gastric wall perforation after upper endoscopy specifically; its rarity therefore cannot be quantified, and the available evidence consists of isolated case reports[3,4,10]. Comparison with the literature on posterior perforated peptic ulcers[3,4] is therefore only partially informative, since those defects arise from a pre-existing mucosal lesion; the shared feature is anatomical rather than etiological, namely decompression into the lesser sac and the resulting attenuation of early peritoneal signs.
The patient’s creatinine rose from a documented baseline of 1.1 mg/dL to 4.18 mg/dL over seven days—in the context of septic peritonitis, severe hypotension, and anuria. This pattern is consistent with sepsis-associated ischemic ATI[9]. CA-AKI—conventionally defined as a ≥ 0.5 mg/dL or ≥ 25% rise in creatinine within 48-72 hours of contrast exposure without an alternative cause—typically peaks at 3-5 days post-contrast and is generally self-limiting[7]. Controlled data indicate that the incidence attributable to intravenous contrast in unselected patients is considerably lower than historically assumed[8]. Given the 7-day interval since contrast administration and the overwhelming hemodynamic insult, contrast exposure is best regarded as a possible contributory factor rather than the primary etiology of AKI in this patient. This attribution nonetheless remains a clinical inference: Urinalysis, urinary microscopy, urinary biomarkers, and renal ultrasonography were not available, and the further contrast load administered at emergency presentation cannot be separated from the septic insult in the subsequent renal trajectory. The documented renal course—a baseline creatinine of 1.1 mg/dL (eGFR 62 mL/minute/1.73 m2) 7 days before admission, anuria with a 3.8-fold rise in serum creatinine at presentation, initiation of CVVH on ICU day 2, and dependence on renal replacement therapy until death without renal recovery—is nevertheless more in keeping with severe sepsis-associated ischemic ATI than with CA-AKI. The patient also had established CA-AKI risk factors, including cardiac disease and prior malignancy[7].
Several factors compounded the diagnostic challenge. Loss of verbal communication due to prosthesis migration prevented the patient from reporting worsening abdominal symptoms during the 3-day interval between endoscopy and presentation. Advanced thoracolumbar scoliosis and pectus carinatum alter visceral positioning and chest wall mechanics, and it is plausible that they attenuated the peritoneal signs expected with perforation. Direct evidence for this specific effect is limited: The available literature addresses abdominal wall muscle asymmetry in adolescent idiopathic scoliosis rather than the reliability of peritoneal signs in adults with fixed thoracolumbar deformity[6], and this claim should therefore be read as a clinical inference rather than an established finding. The combination of these factors—posterior perforation anatomy, structural deformities, and a nonverbal patient—created conditions in which a life-threatening complication could progress largely undetected for 72 hours.
The complexity of this case extended well beyond the initial presentation. A jejunostomy-related bile leak necessitated re-laparotomy and additional bowel resection with stoma formation. The drain-induced ileal wall injury identified at the second surgery underscores the vulnerability of surgically altered, malnourished bowel in the setting of prolonged inflammation. Histopathology of the resected small bowel also showed ischemic necrosis at the surgical margins, which raises the possibility that ischemic injury extended beyond the resected segment and may have contributed to the subsequent deterioration. The two intracardiac thrombi—in the left atrium and at the left ventricular apex—were incidental but clinically important findings in a patient with atrial fibrillation and profound systemic inflammation and were managed with anticoagulation without surgical intervention. Despite aggressive multidisciplinary management, the accumulated burden of septic shock, multiorgan failure, prior malignancy-related deconditioning, and repeated surgical insult proved unsurvivable. The relative contribution of the 72-hour delay in source control to this cascade cannot be quantified from a single case; the later complications were most probably multifactorial, reflecting pre-existing deconditioning, prolonged peritoneal inflammation, and the technical demands of repeated surgery in a hostile abdomen.
This report has several limitations. First, it describes a single patient, so no causal inference can be drawn. Second, the perforation was not visualized endoscopically, and no immediate post-procedure imaging was performed, so both the timing and mechanism of injury remain inferential; in particular, the relative contributions of scope advancement against resistance, esophageal dilation, biopsy, and insufflation cannot be distinguished. Third, the renal diagnostic assessment was limited to serial serum creatinine, urine output, and eGFR; urinalysis, urinary microscopy, urinary biomarkers, and renal imaging were not available, so the diagnosis of sepsis-associated ischemic ATI is clinical rather than biopsy- or biomarker-confirmed. Fourth, this is a retrospective single-center report, and detailed serial laboratory, microbiological, hemodynamic, and renal replacement therapy parameters could not be retrieved in a form suitable for reporting; consequently, sepsis severity scores, serial lactate values, microbiological culture results, and the doses and durations of antimicrobial and vasopressor therapy are not reported, and the adequacy of source control and antimicrobial therapy cannot be formally assessed. No autopsy was performed. These limitations should be borne in mind when interpreting the mechanistic interpretations offered above.
This case represents a diagnostically and surgically complex presentation of posterior gastric perforation following endoscopy in a patient with extensive comorbidities (Table 1). The 3-day delay between the procedure and presentation, atypical physical signs attributable to structural deformities and communication barriers, and the multifactorial nature of AKI—dominated by sepsis-associated ischemic ATI rather than CA-AKI—illustrate the pitfalls of applying standard clinical patterns to high-risk patients. A low threshold for early cross-sectional imaging and early multidisciplinary involvement may be warranted in patients with unexplained deterioration following upper gastrointestinal endoscopy, particularly when altered anatomy or impaired communication limits clinical assessment. In our experience, the features that should prompt urgent contrast-enhanced CT rather than observation are unexplained hypotension, new oliguria or anuria, a disproportionate inflammatory response, or any unexplained clinical deterioration within the first week after the procedure. A single case cannot establish an imaging threshold or confirm a mechanism of injury, and these observations should be regarded as hypothesis-generating rather than as recommendations supported by comparative evidence.
| Time point | Event and key findings |
| Day -7 | Contrast-enhanced CT of the neck, thorax, and abdomen for oncological surveillance. Serum creatinine 1.1 mg/dL, eGFR 62 mL/minute/1.73 m2. No new pathology identified |
| Day -3 | Upper gastrointestinal endoscopy for feeding difficulty. Tracheoesophageal voice prosthesis found migrated into the esophageal lumen; scope advanced with resistance posterior to the device. Bougie dilation of a proximal esophageal stricture; five gastric biopsies (prepyloric region, antrum, incisura angularis, greater curvature, and lesser curvature) obtained. Chronic active gastritis with H. pylori. No perforation or immediate complication documented |
| Day -3 to day 0 | At home. No reliable symptom history obtainable because of nonverbal status |
| Day 0 (admission) | Emergency department arrival by ambulance with syncope. BP 84/50 mmHg, SpO2 88%, anuria. Creatinine 4.18 mg/dL (KDIGO stage 3 AKI), BUN 103 mg/dL, CRP 359 mg/L, K+ 6.56 mEq/L, pH 7.19. Contrast-enhanced abdominal CT: Posterior gastric wall perforation with contrast extravasation, free air, and four-quadrant free fluid |
| Day 0 (same day) | Emergency laparotomy: Four-quadrant bile-stained contamination; 2.5-cm full-thickness defect of the posterior wall of the gastric corpus. Gastric wedge resection, Witzel feeding jejunostomy, and four drains. Intraoperative endoscopy: Voice prosthesis in its expected esophageal position. Histopathology: Mucosal erosion, submucosal hemorrhage and edema with perforation; no ulcer or neoplasia; H. pylori not identified |
| Postoperative day 1 | Admission to the ICU; mechanical ventilation via tracheostomy, vasopressor support, and broad-spectrum antimicrobial therapy |
| Postoperative day 2 | CVVH started for refractory oliguria and azotemia; continued until death without renal recovery |
| ICU follow-up | CT: Left atrial thrombus (17 mm × 10 mm) and periportal fluid collection (63 mm × 34 mm). Transthoracic echocardiography: Separate left ventricular apical thrombus, with preserved systolic function. Therapeutic low-molecular-weight heparin started; no urgent cardiovascular surgical intervention indicated. Potassium normalized to 4.2 mEq/L |
| Postoperative day 10 | Bile in the abdominal drains. Re-laparotomy: Detachment of the jejunostomy catheter with bile leakage; gastric staple line intact. Jejunal resection with side-to-side anastomosis, double-barrel ileostomy for drain-related ileal injury, surgical (Pezzer) gastrostomy, and three new drains. Histopathology: 1-cm perforation, active serositis, and ischemic necrosis at the surgical margins |
| Postoperative day 16 (April 30, 2025) | Death in the ICU from refractory multiorgan failure. As the index operation was performed on the day of admission, postoperative day 16 corresponded to hospital day 16 |
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