Post-cesarean pneumoperitoneum beyond expected revealing a sealed cecal perforation: a case report

Abstract

Background

Small volumes of intraperitoneal air can follow cesarean delivery, but persistence or progression beyond the immediate postoperative period is unusual and may indicate hollow-viscus injury.

Case presentation

A 30-year-old gravida 5, para 3, abortus 1 Palestinian female with prior right ovarian cystectomy underwent an uncomplicated elective lower-segment cesarean section and was discharged on postoperative day 2. She re-presented on postoperative day 4 with colicky abdominal pain, distension, and subjective fever. The examination showed tachycardia and a distended, tympanitic abdomen with a clean Pfannenstiel incision. The inflammatory markers and leukocyte count rose. Computed tomography demonstrated pneumoperitoneum greater than expected postoperatively with diffuse bowel dilatation and mild free fluid; repeat computed tomography on postoperative day 6 showed progression. Oral-contrast computed tomography showed no extravasation. Peritoneal aspiration yielded turbid fluid that cultured extended-spectrum β-lactamase-producing Escherichia coli. As the isolate demonstrated sensitivity to gentamicin, the empiric aminoglycoside was continued incombination with metronidazole. This regimen was maintained until surgery, as advised by the infectious diseases team. Given concern for occult perforation, exploratory laparotomy on postoperative day 10 revealed fibrinous peritonitis and an approximately 2-cm sealed cecal perforation with healthy margins. Primary repair with appendectomy and drainage was performed. Early postoperative recovery was stable.

Conclusion

Progressive post-cesarean pneumoperitoneum, even with a negative contrast study, should prompt a high index of suspicion for concealed bowel perforation. Correlating serial imaging with inflammatory markers and peritoneal fluid analysis can guide timely intervention. When identified early, and when intraoperative contamination is limited, bowel-preserving primary repair with drainage can achieve favorable maternal outcomes.

Introduction

Cesarean delivery is among the most frequently performed operations worldwide. Although generally safe, postoperative morbidity remains clinically relevant. Surgical site infection occurs in an estimated 5.6% of cesarean deliveries globally, with regional variation and Staphylococcus aureus and Escherichia coli among the most common pathogens [1]. Urologic injuries are uncommon but important; pooled estimates suggest bladder injury occurs in ~267 per 100,000 cesarean procedures and ureteric injury in ~9 per 100,000 [2]. Post-cesarean paralytic ileus is infrequent as the incidence of it was 135 in a study included 23,486 patients (0.6%), but is associated with increased short-term maternal morbidity and can complicate early postpartum assessment [3].

By contrast, gastrointestinal injury after cesarean delivery is rare. Reported estimates place iatrogenic gastrointestinal perforation around 0.08%, and postpartum functional bowel disorders such as acute colonic pseudo-obstruction (Ogilvie syndrome) can precipitate cecal perforation in the absence of mechanical obstruction [4, 5]. We report early postpartum peritonitis from a sealed cecal perforation after cesarean delivery. This case shows how ileus-like symptoms can mask intra-abdominal sepsis and supports a low threshold for computed tomography (CT) and early surgical evaluation when pain or gastrointestinal dysfunction persists postpartum, broadening the differential to include sealed colonic perforation.

Case presentation

A 30-year-old Palestinian woman (gravida 5, para 3, abortus 1) with no chronic illnesses and no known drug allergies presented in the immediate postpartum period. Her history included a prior laparotomy for right ovarian cystectomy 5 years earlier. The body mass index was 25. Antenatal imaging had shown fetal intracranentricular hemorrhage (IVH) with ventriculomegaly: ultrasound identified a hypoechoic lesion beneath the left choroid plexus and periventricular calcification, and fetal brain magnetic resonance imaging reported IVH, ventriculomegaly with possible posthemorrhagic hydrocephalus or ex-vacuo dilatation, and agenesis of the corpus callosum. A plan for cesarean delivery was made. She underwent an elective lower-segment cesarean section (index operation; postoperative day [POD] 0). Estimated blood loss was 600 mL, and the operative note stated no adhesions and no postpartum hemorrhage. Postoperative care over the first 2 days included intravenous fluids, intravenous antibiotics, and analgesia. She was discharged home on POD 2 with oral antibiotics, a laxative, and oral analgesics. The neonate was admitted to the neonatal intensive care unit. On POD 4 she returned with progressive colicky abdominal pain, abdominal distension/bloating, and subjective fever/chills; she denied vomiting, urinary symptoms, heavy vaginal bleeding, upper respiratory symptoms, or headache. Vital signs showed blood pressure 127/75 mmHg, heart rate 110/min, respiratory rate 16/min, axillary temperature 37 °C, and oxygen saturation 97% on room air. She appeared well. The abdomen was distended and tympanitic with tenderness limited to the incision on deep palpation; bowel sounds were present. The Pfannenstiel incision was clean. Pelvic ultrasound showed a bulky empty uterus with mild–moderate free fluid; pelvic examination noted normal lochia. Breast examination showed symmetric warm engorgement with intact nipples.

Key investigations started on POD 4. Laboratory tests showed: hemoglobin 9.8 g/dL (trend: 9.9 on POD 5; 10.2 POD 6; 10.3 POD 7; 9.7 POD 8; 10.0 POD 9; 10.1 POD 10) (Fig. 1C), white blood cell (WBC) count 12.9 → 14.6 → 13.3 × 10⁹/L (PODs 4–6), platelets 334 × 10⁹/L (Fig. 1A), C-reactive protein (CRP) 191 → 470 →  > 480 mg/L (PODs 4–6) (Fig. 1B), international normalized ratio 1.08, potassium 3.8 mmol/L, blood urea nitrogen 6 mg/dL, creatinine 0.5 mg/dL, aspartate aminotransferase 19 U/L, and alanine aminotransferase 9 U/L.

Fig. 1.

A–C Serial laboratory trends during readmission. A–C show WBC count (× 10⁹/L), hemoglobin (g/dL), and C-reactive protein (mg/L) from postoperative day 4–10. Points indicate measured draws; lines connect consecutive observations; vertical dotted lines mark readmission (postoperative day 4) and pre-operative assessment (postoperative day 10). C-reactive protein on postoperative day 6 was reported as “> 480 mg/L” and is plotted at the assay upper limit with a “>” annotation

Table 1 summarizes the landmark laboratory findings during the postoperative period. CRP demonstrated a sharp rise, peaking at > 480 mg/L on POD 6, consistent with a pronounced inflammatory response. WBC peaked at 14.6 × 10⁹/L on POD 5 but remained within a moderate range, while hemoglobin levels showed minimal variation, reaching a nadir of 9.7 g/dL on POD 8 and stabilizing at 10.1 g/dL preoperatively. These values reflect the systemic response and hematological changes leading up to re-operation.

Table 1.

Landmark laboratory values (first, peak/nadir, last value before operation)

Test (units)	First value (POD)	Peak value (POD)	Nadir value (POD)	Last pre-op (POD)
CRP (mg/L)	191 (4)	> 480 (6)	–	–
WBC (× 10⁹/L)	12.9 (4)	14.6 (5)	12.9 (4)	–
Hemoglobin (g/dL)	9.8 (4)	10.3 (7)	9.7 (8)	10.1 (10)

Chest radiograph was clear; an upright abdominal radiograph showed distended bowel loops with air–fluid levels. Contrast-enhanced computed tomography (CT) of the abdomen/pelvis on POD 4 demonstrated moderate pneumoperitoneum greater than expected postoperatively, diffuse small and large bowel dilatation (ileus), ileal wall thickening, and mild free intraperitoneal fluid without abscess/collection (Fig. 2).

Fig. 2.

Computed tomography abdomen/pelvis on postoperative day 4: the arrows point to a moderate pneumoperitoneum layering in the rectouterine pouch (pouch of Douglas), greater than expected for the early post-cesarean state

Initial inpatient management (POD 4) included empiric antimicrobials—ampicillin 2 g intravenous every 6 h, metronidazole 500 mg intravenous every 8 h, and gentamicin 80 mg intravenous every 8 h—together with enoxaparin 40 mg subcutaneously daily and paracetamol 1 g intravenous every 6 h, because the peritoneal fluid culture grew extended-spectrum β-lactamase (ESBL) Escherichia coli susceptible to gentamicin, we narrowed to targeted therapy—continuing gentamicin with metronidazole for anaerobic coverage on infectious-diseases advice, and maintained this regimen until surgery.

A repeat contrast-enhanced CT on POD 6 showed worsening pneumoperitoneum and increased free fluid. The radiologist recommended a rectal-contrast CT to assess for colonic leak; however, due to limited availability and patient tolerance at the external hospital, a CT with oral contrast was performed instead. The oral-contrast CT revealed no extravasation (Fig. 3).

Fig. 3.

CT abdomen/pelvis on postoperative day (POD) 6: the arrows point to a moderate low-attenuation fluid is present throughout the abdomen and pelvis, increased compared with the prior study. In the right lower abdomen and posterior to the uterus, the collection is more loculated, measuring up to 9.5 × 9.0 cm

Despite a negative oral-contrast CT, the combination of rising inflammatory markers and increasing free intraperitoneal air maintained a high clinical suspicion for occult hollow-viscus perforation. Diagnostic peritoneal aspiration was performed while the patient remained admitted, on post-operative day (POD) 6 at an external hospital yielded turbid yellow fluid (pH 8) with leukocytes 14 (95% neutrophils, 5% lymphocytes), erythrocytes 25, protein ratio 0.7, and lactate dehydrogenase ratio 20; culture grew extended-spectrum β-lactamase (ESBL) producing Escherichia coli sensitive to meropenem, gentamicin, levofloxacin, and piperacillin–tazobactam. The contemporaneous working differential included post-cesarean paralytic ileus, acute colonic pseudo-obstruction (Ogilvie syndrome) with cecal distension, and hollow-viscus injury/leak; stercoral perforation and ischemic colitis were considered less likely.

On POD 10, she underwent exploratory laparotomy for suspected perforation. Intraoperative findings were fibrinous peritonitis with multiple loculated pockets and adhesions requiring adhesiolysis, and an approximately 2 cm sealed cecal perforation with a healthy base. Primary repair was performed with interrupted sutures; appendectomy was done for secondary inflammation. Three hemovac drains were placed (left upper quadrant/splenic area, right upper pelvis, and right lower Morison’s pouch). Postoperatively, she received nasogastric decompression with nil per os, intravenous fluids, analgesia, and antiplatelet therapy (acetylsalicylic acid) per the surgical team, the decision to introduce aspirin was made by the surgical team as part of their postoperative protocol. The immediate postoperative course was stable; she was afebrile with no initial drain output Table 2.

Table 2.

Clinical timeline relative to the index cesarean

Time	Key symptoms/findings	Diagnostics	Interventions/outcome
POD 0 (index operation)	Elective lower-segment cesarean; early postpartum recovery on ward	–	Routine postoperative care; oral analgesia
POD 1–2	Routine postpartum course	–	Discharge plan; neonate admitted to NICU
POD 4 (readmission)	Progressive colicky abdominal pain, distension/bloating; subjective fever/chills	Labs: leukocytosis; rising CRP. Upright abdominal radiograph: bowel dilatation and free air. CT: pneumoperitoneum greater than expected	Empiric broad‑spectrum antimicrobials; inpatient monitoring
POD 6	Ongoing symptoms	Repeat CT: worsening pneumoperitoneum and fluid; radiologist suggested rectal‑contrast CT. Oral‑contrast CT: no contrast extravasation. Peritoneal aspiration: turbid fluid; neutrophil‑predominant; culture: ESBL E. coli	Continued antibiotics; surgical re‑evaluation given discordant imaging versus clinical trajectory
POD 10	Worsening inflammatory markers; persistent free air	–	Exploratory laparotomy: fibrinous peritonitis; ~ 2‑cm sealed cecal perforation. Primary repair + appendectomy + drainage; early postoperative course stable

At 2 weeks postoperatively, the incision was clean, dry, and intact, and bowel function had normalized. At 6-week postoperative clinic review (post-laparotomy), the patient reported improving pain with return of normal bowel function and activity. Examination showed a well-healed Pfannenstiel incision without hernia or tenderness.

Regarding the neonate, no further details are available as neonatal management was transferred to the pediatric team immediately after delivery and was not directly related to the index maternal case.

Discussion

Persistent or progressive pneumoperitoneum after cesarean delivery is unusual and should not be attributed solely to residual postoperative air. While often mild and self-limiting, its persistence or progression, as seen in our patient and others [4, 5] is a critical indicator of a major surgical complication such as hollow viscus perforation. Typical symptoms of gastrointestinal perforation include abdominal pain, distension, fever, and leukocytosis, many of which were present in our patient. However, these findings are nonspecific and can be mistaken for benign postoperative changes such as acute colonic pseudo-obstruction (Ogilvie’s syndrome), iatrogenic bowel injury, and paralytic ileus. Differentiating benign postoperative pneumoperitoneum from clinically significant bowel injury is inherently challenging. Conventional imaging modalities can be inconclusive, oral contrast studies may fail to reveal contained or sealed perforations, and CT interpretation requires close correlation with clinical and biochemical data. In our patient, serial CTs demonstrated progressive free air, while C-reactive protein levels rose sharply, and diagnostic peritoneal aspiration revealed neutrophil-predominant fluid with positive culture. The convergence of these findings strengthened the suspicion for bowel perforation despite a negative oral contrast study and justified surgical re-exploration.

A comparison of the two cases [4, 5], in addition to the present case, reveals critical differences in presentation and management that guided surgical decision-making Table 3. The timing of symptom onset differed between cases. In case 1 [4], symptoms appeared on the first postoperative day, while in case 2 [5] they worsened within 24–48 h. By contrast, our patient developed symptoms on postoperative day 4. This highlights that although the risk for this complication is highest early on, it can persist well beyond the early recovery phase.

Table 3.

Summary of reported cases of post-cesarean gastrointestinal perforation

References	Timing of symptoms	Type of perforation	Management	Outcome
Khajehnoori and Nagra [4]	POD 1	Free perforation with fecal peritonitis	Ileocolic resection + diverting stoma	Good postoperative recovery
Schweitzer et al. [5]	POD 2 (24–48 h)	Contained perforation, less contamination	Ileocecal resection + primary anastomosis	Uneventful recovery
Present case	POD 4	Sealed cecal perforation with localized fibrinous peritonitis	Primary repair + drainage (bowel preserved)	Favorable recovery

The extent and severity of the perforation were a key differentiating factor, directly influencing the choice of surgical procedure. In case 1 [4], the presence of free perforation with fecal peritonitis necessitated the most aggressive intervention—an ileocolic resection with a diverting stoma. This strategy is the standard of care when there is uncontrolled contamination, as it helps control sepsis and promotes healing. Case 2 [5], however, was managed with an ileocecal resection and primary anastomosis, reflecting a more contained situation with less contamination, where a primary connection was considered safe. By contrast, our patient had the mildest presentation—a sealed perforation with localized fibrinous peritonitis. This allowed for a more conservative approach: primary repair of the perforation with drainage, thereby preserving full bowel continuity.

Operative management must be tailored to the intraoperative findings. Extensive peritoneal soilage or tissue necrosis generally necessitates resection and diversion, whereas contained perforations with viable margins may be amenable to direct repair and drainage. In our case, the decision to proceed with primary closure of the cecal defect was supported by the limited contamination and healthy tissue observed. More broadly, this case underlines the importance of integrating radiological, laboratory, and bedside clinical information when determining the timing of surgical exploration.

Limitations and conclusions

This report is limited by its single-case design and the absence of long-term neonatal outcome data. Nevertheless, several important lessons emerge: persistent pneumoperitoneum after cesarean delivery should not be dismissed; diagnostic peritoneal aspiration can provide valuable complementary evidence when imaging is inconclusive; and early multidisciplinary reassessment can facilitate bowel-preserving surgical management. Collectively, these points highlight the need for heightened vigilance and a low threshold for re-exploration in similar postoperative scenarios.

Conclusion

Progressive or persistent pneumoperitoneum after cesarean delivery should trigger suspicion for concealed bowel injury even when contrast studies are negative. Triangulating serial CT findings with inflammatory markers and, when needed, peritoneal fluid analysis supports timely escalation and can justify early exploration. When contamination is limited and tissue is viable, primary repair with drainage can avert resection/diversion and yield favorable maternal recovery. Postpartum teams should adopt trigger-based pathways for re-imaging and early surgical consultation and consider diagnostic peritoneal aspiration when imaging is equivocal. Prospective registries should be developed to define radiographic/biochemical thresholds that distinguish benign postoperative air from pathology, as should comparative studies of early exploration versus nonoperative management on morbidity, length of stay, and fertility outcomes.

Author contributions

TQ: collected clinical data, contributed to the literature review, and drafted the initial manuscript. HQ: assisted in data collection, literature review, and critical revision of the manuscript. MY: contributed to manuscript writing, editing, and data interpretation. LA: assisted with literature review and provided critical feedback on the discussion. GMB: assisted in manuscript revision and provided clinical input. IB: supervised the case report, contributed to the conception and design, critically revised the manuscript, and approved the final version. All authors read and approved the final manuscript.

Funding

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Data availability

All data supporting the findings of this study are included within the article. Additional de-identified clinical information is available from the corresponding author upon reasonable request.

Declarations

Ethics approval and consent to participate

Ethical approval was not required for a single case report according to the policies of our institution.

Consent for publication

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal upon request.

Competing interests

The authors declare that there is no conflict of interest regarding the publication of this article.