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International Medical Case Reports Journal logoLink to International Medical Case Reports Journal
. 2026 Sep 29;19:632789. doi: 10.2147/IMCRJ.S632789

Neonatal Gastric Perforation Temporally Associated with Nasogastric Tube Insertion: A Case Report

Shukri Said Mohamed 1, Omar Adam Sheikh 2,✉, Ahmet Sarac 3, Abdisamad Omar Ali 1, Abdirahman Ahmed Mohamud 4, Abdullahi Ali Moallim Hussien 5
PMCID: PMC13633743  PMID: 42829737

Abstract

Background

Neonatal gastric perforation (NGP) is a rare but potentially life-threatening condition associated with substantial morbidity and mortality. Approximately half of reported cases are idiopathic or spontaneous, while the remainder are attributed to identifiable causes, including congenital gastric wall defects, hypoxic-ischemic injury, and iatrogenic trauma related to nasogastric tube (NGT) insertion, particularly in premature and low-birth-weight infants. Early diagnosis and prompt surgical intervention are critical for improving outcomes. We report a case of gastric perforation temporally associated with nasogastric tube insertion in a preterm, small-for-gestational-age (SGA) neonate, highlighting the diagnostic challenge of distinguishing mechanical from ischemic etiologies, together with management and preventive considerations.

Case Presentation

We describe a male preterm neonate, born at 34 weeks of gestation with a birth weight of 1.5 kg (small for gestational age), who developed acute abdominal distension and respiratory distress approximately 12 hours after nasogastric tube placement for enteral feeding. Abdominal radiography revealed significant pneumoperitoneum, indicating gastrointestinal perforation. Emergency exploratory laparotomy confirmed a 1-cm full-thickness gastric perforation along the greater curvature of the stomach. The perforation was repaired surgically, and the infant subsequently recovered with comprehensive postoperative intensive care management.

Conclusion

Clinicians should maintain a high index of suspicion for gastric perforation in neonates, particularly those born preterm or small for gestational age, who develop rapid abdominal distension, pneumoperitoneum, or signs of sepsis following nasogastric tube insertion. Because clinical and radiological findings alone often cannot reliably distinguish mechanical from ischemic causes, standardized insertion protocols, prompt radiological evaluation, and timely surgical intervention remain essential for improving survival and outcomes in this rare but serious condition.

Keywords: neonatal gastric perforation, nasogastric tube, iatrogenic injury, prematurity, small for gestational age, intrauterine growth restriction, pneumoperitoneum

Introduction

Neonatal gastric perforation (NGP) is a rare but life-threatening surgical emergency that accounts for approximately 7% of gastrointestinal perforations in neonates and remains associated with considerable morbidity and mortality despite advances in neonatal intensive care and pediatric surgery.1,2 The condition most commonly occurs during the first week of life and has been reported in both term and preterm infants, with prematurity and low birth weight consistently identified as important prognostic factors.1,2

Reported series suggest that roughly half of NGP cases are idiopathic or spontaneous, with the remainder attributed to identifiable causes.3 Proposed etiological mechanisms for the latter group include congenital defects of the gastric musculature, ischemic injury secondary to hypoxia, increased intragastric pressure from positive-pressure ventilation, distal gastrointestinal obstruction, and iatrogenic trauma.1 Among iatrogenic causes, injury related to nasogastric tube (NGT) insertion has been recognized as a rare but clinically significant mechanism, particularly in fragile premature infants with underdeveloped gastric wall structures.1,3

The immature neonatal stomach appears to be vulnerable to both mechanical and ischemic injury. Anatomically, the muscularis propria, particularly the circular muscle layer near the fundus and greater curvature, matures relatively late in gestation, leaving these regions with reduced tensile strength and resilience.3 Mechanistically, repeated instrumentation, excessive insertion force, or malpositioning of the tube tip may generate localized pressure and mucosal erosion that can progress to full-thickness injury if the tip repeatedly abuts the thin gastric wall, although this sequence is rarely confirmed radiologically or intraoperatively.1,4 Separately, infants born preterm or small for gestational age (SGA) may experience systemic hypoxia and splanchnic hypoperfusion, which predispose the stomach, particularly the watershed area along the greater curvature, to focal ischemic necrosis independent of any instrumentation.3 Distinguishing between these mechanical and ischemic pathways is often difficult in an individual case, and both should be considered when a growth-restricted preterm infant develops perforation shortly after NGT placement.

Nasogastric tube placement is routinely performed in neonatal intensive care units (NICUs) for enteral feeding and gastric decompression. Although generally considered safe, mechanical complications may occur, including malposition, mucosal injury, and, rarely, full-thickness perforation. Notably, most reported iatrogenic NGT-related perforations in neonates involve the esophagus rather than the stomach, underscoring the relative rarity of the gastric complication described here.5

Clinically, NGP typically presents with sudden abdominal distension, feeding intolerance, respiratory deterioration, and radiographic evidence of massive pneumoperitoneum. Because disease progression can be rapid and catastrophic, early diagnosis and prompt surgical intervention remain critical determinants of survival. Recent studies continue to emphasize the importance of rapid recognition and multidisciplinary management to improve clinical outcomes.2,6,7

We report a case of gastric perforation temporally associated with nasogastric tube insertion in a preterm, small-for-gestational-age neonate, with the aim of highlighting the diagnostic challenge of distinguishing mechanical from ischemic etiologies and reinforcing safe NGT insertion practices in this high-risk population.

Case Presentation

A male neonate was born at 34 weeks of gestation by normal vaginal delivery, with a birth weight of 1.5 kg, meeting the criteria for small-for-gestational-age status. His Apgar scores were 5 and 9 at 1 and 5 minutes, respectively. He was admitted to the neonatal intensive care unit (NICU) for management of respiratory distress and received respiratory support with continuous positive airway pressure (CPAP).

On the third day of life, an 8-Fr polyvinyl chloride (PVC) nasogastric tube was inserted according to the unit’s standard feeding protocol to facilitate enteral feeding. Resistance was encountered during insertion, and tube position was checked by auscultation before feeding was initiated.

Approximately 12 hours after tube placement, the infant developed progressive abdominal distension accompanied by tachypnea and lethargy. Physical examination revealed a markedly distended and rigid abdomen with absent bowel sounds. The infant was semiconscious and clinically unstable, with a respiratory rate of 65 breaths/min, blood pressure of 45/20 mmHg, temperature of 38.0°C, heart rate of 200 beats/min, and oxygen saturation of 85%.

An urgent abdominal radiograph demonstrated a large amount of free intraperitoneal air, consistent with pneumoperitoneum and highly suggestive of gastrointestinal perforation (Figure 1). Laboratory investigations revealed metabolic acidosis, with an arterial blood gas showing a pH of 7.20, PaCO2 of 30 mmHg, and HCO3− of 19 mEq/L. Serum sodium was 136 mmol/L, potassium was 2.5 mmol/L, and hemoglobin was 12 g/dL. Inflammatory markers were also elevated.

Figure 1.

An X-ray image showing the skeletal structure of a small animal, with ribs and spine visible.

Plain abdominal radiograph showing massive pneumoperitoneum with extensive free intraperitoneal air beneath the diaphragm and throughout the abdominal cavity, suggestive of gastric perforation.

Given the clinical and radiological findings, the patient underwent emergency exploratory laparotomy. Intraoperatively, a 1-cm full-thickness perforation was identified along the greater curvature of the stomach (Figure 2). No additional gastrointestinal abnormalities or intestinal perforations were observed. The gastric defect was repaired primarily using 2–0 polyglactin (Vicryl) sutures in a single layer, followed by 3–0 polyglactin (Vicryl) sutures in a double-layer Lembert technique (Figure 3). Thorough peritoneal lavage was subsequently performed. Histopathological examination of the perforation margins was not performed.

Figure 2.

Intraoperative view of an anterior gastric perforation (arrow) along the greater curvature, exposed by surgical retractors.

Intraoperative photograph demonstrating an anterior full-thickness gastric perforation (arrow) located along the greater curvature of the stomach, identified during exploratory laparotomy.

Figure 3.

Intraoperative view of gastric perforation repair with interrupted sutures and double-layer Lembert reinforcement.

Intraoperative photograph demonstrating primary repair of the gastric perforation using 2–0 polyglactine vicryl in an interrupted sutures and followed by reinforcement 3–0 polyglactine vicryl in a with a double-layer lembert suture technique (arrow) to ensure secure closure of the gastric wall defect.

Postoperatively, the neonate was managed in the NICU with broad-spectrum antibiotics, total parenteral nutrition, respiratory support, and careful fluid and electrolyte monitoring. Over the subsequent two weeks, the infant demonstrated gradual clinical improvement, with resolution of the abdominal symptoms and successful reintroduction of enteral feeding via a nasogastric tube. Follow-up abdominal radiography showed complete resolution of the pneumoperitoneum, with no evidence of recurrent perforation. The patient was discharged in stable condition after achieving full feeding tolerance and satisfactory recovery, following a total hospital stay of 15 days, at a corrected gestational age of 36 weeks.

Discussion

Neonatal gastric perforation remains an uncommon but devastating condition requiring immediate recognition and treatment. Although spontaneous perforation has historically been considered the predominant form, increasing awareness of iatrogenic causes has highlighted the role of invasive neonatal procedures, including NGT insertion, which most commonly affects the esophagus but, rarely, may also involve the stomach, as in the present case.1,5 The present case contributes to the growing body of evidence demonstrating that routine bedside procedures may occasionally result in severe gastrointestinal complications.

The precise mechanism of NGT-associated gastric perforation remains uncertain. Direct mechanical trauma is considered a plausible explanation in many reported cases, particularly when perforation develops shortly after tube placement; however, in the absence of radiologic confirmation of tube malposition, a “punched-out” mucosal defect, or histopathological evidence of tube trauma, a purely temporal association cannot be equated with proven mechanical causation. Prematurity, low birth weight, hypoxia, and immature gastric wall development may further increase vulnerability to injury, whether the ultimate mechanism is mechanical or ischemic. Chen et al, in a systematic review of 168 reported cases, identified prematurity as a significant predictor of mortality and demonstrated that preterm infants tend to develop perforation earlier than term neonates.1 More recently, Ong et al highlighted several potentially preventable risk factors and reinforced the importance of meticulous clinical monitoring in high-risk infants.8

This literature also underscores a distinction directly relevant to the present case: differentiating true mechanical (iatrogenic) perforation from focal ischemic or congenital muscular-defect perforation, which is particularly important in a growth-restricted preterm infant such as ours.3 In addition, ex vivo modeling of neonatal gastric tubes has shown that tube stiffness and material influence both the ease of insertion and the risk of malposition against the gastric wall, with softer tubes associated with more favorable behavior, suggesting a modifiable, device-related contributor to injury risk.9

The clinical presentation of NGP is often abrupt. Progressive abdominal distension remains the most consistent clinical finding and is frequently accompanied by respiratory distress, feeding intolerance, vomiting, metabolic derangements, and hemodynamic instability. Massive pneumoperitoneum identified on plain abdominal radiography remains the hallmark diagnostic finding and often provides the first indication of gastrointestinal perforation. Recent reports continue to emphasize the value of early imaging in facilitating prompt diagnosis and reducing treatment delays.2,6

Mortality associated with NGP remains substantial despite improvements in neonatal care. Recent predictive modeling studies have reported mortality rates ranging from approximately 20% to 30%, with adverse outcomes associated with hypoxia, metabolic acidosis, coagulation abnormalities, thrombocytopenia, and delayed intervention.6 These findings support previous observations that rapid recognition and timely surgical management are essential determinants of survival.1

Surgical repair remains the standard treatment for most cases of NGP. Primary closure following laparotomy is generally effective when viable gastric tissue is present and diagnosis is established early. Delayed treatment may result in extensive peritoneal contamination, sepsis, multiorgan dysfunction, and increased mortality. Accordingly, prompt operative management combined with comprehensive neonatal intensive care support remains the cornerstone of treatment.1,6

The present case underscores several important clinical lessons. First, clinicians should maintain a high index of suspicion for gastric perforation when sudden abdominal distension develops shortly after NGT insertion, while recognizing that ischemic mechanisms in SGA infants remain part of the differential diagnosis. Second, standardized insertion techniques, including measured insertion length, use of softer catheter materials, and objective confirmation of tube position by pH aspirate testing or radiography rather than auscultation alone are reasonable preventive measures.9 Finally, rapid multidisciplinary collaboration involving neonatologists, pediatric surgeons, anesthesiologists, and intensive care specialists is crucial for optimizing patient outcomes, including early surgical consultation and, when clinically indicated, emergent needle decompression of tension pneumoperitoneum to stabilize the infant prior to definitive laparotomy.

Limitations

This report has several limitations. First, the diagnosis of iatrogenic mechanical perforation was based on clinical and intraoperative findings rather than on pre-insertion baseline gastric imaging or histopathological examination of the perforation edges; a contribution from focal ischemic necrosis related to prematurity and growth restriction therefore cannot be excluded. Second, procedural details relevant to mechanism including the exact NGT material and caliber, the number of insertion attempts, and the method used to verify tube position were not systematically documented at the time of placement. Third, as a single observational case, this report cannot be used to estimate incidence or to generalize preventive protocols; larger prospective series are needed to clarify the relative contribution of mechanical and ischemic mechanisms in this population.

Conclusion

Gastric perforation temporally associated with nasogastric tube insertion is a rare but potentially life-threatening complication in neonates, particularly those born preterm or small for gestational age, in whom an immature gastric wall and coexisting ischemic vulnerability may increase susceptibility to injury. Because clinical and radiological findings alone often cannot distinguish mechanical from ischemic causes, this case supports several specific, actionable practice points. First, NGT placement should follow a standardized measurement protocol (eg, nose-ear-xiphoid or nose-ear-mid-umbilicus distance) to avoid over-insertion and tip malposition in a small gastric cavity, with tube position confirmed by pH aspirate testing and/or radiography rather than auscultation alone. Second, soft polyurethane or silicone catheters should be preferred over stiffer materials for enteral access in high-risk preterm and SGA infants to minimize mechanical mucosal trauma.9 Third, any sudden abdominal distension, feeding intolerance, or unexplained respiratory deterioration following NGT insertion, even hours after placement, should prompt immediate upright or left lateral decubitus abdominal radiography to exclude perforation before further enteral feeds are given. Finally, early pediatric surgical consultation, with emergent needle decompression of the peritoneal cavity for tension pneumoperitoneum when clinically indicated, should precede definitive laparotomy to stabilize the infant hemodynamically and respiratorily. Further studies are needed to better define the incidence of NGT-associated gastric perforation, clarify its relative contribution compared with ischemic and congenital mechanisms, and validate preventive protocols in neonatal intensive care settings.

Acknowledgments

We would like to thank all the participants and Mogadishu Somali Turkish Recep Tayyip Erdoğan Research and Training Hospital for all contributions, corrections, and critical reviews.

Funding Statement

We declare that we have not received any funding support.

Ethical Approval

Based on the regulations of the review board of the Mogadishu Somali Turkish Recep Tayyip Erdoğan Research and Training Hospital, institutional review board approval is not required for case reports. The report was nonetheless conducted in accordance with the ethical principles of the Declaration of Helsinki.

Consent for Publication

Written informed consent for publication of this case report and any accompanying images was obtained from the patient’s parent.

Disclosure

No conflicts of interest in this work.

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