Xinxing Liu
Tingliang Fu
Donghua Li2- 1Department of Pediatric Surgery, Binzhou Medical University Hospital, Binzhou, Shandong, China
- 2Department of Anesthesiology, Binzhou Medical University Hospital, Binzhou, Shandong, China
Spontaneous splenic rupture in children is a rare condition with limited documented cases in the medical literature. It can occur in both enlarged and normal-sized spleens. Clinical manifestations may include abdominal pain, splenomegaly, diminished or absent bowel sounds, Kehr's sign, Ballance's sign, and abdominal guarding. Imaging studies (computed tomography and ultrasound) serve as crucial diagnostic tools for splenic rupture. Splenectomy is no longer considered standard treatment due to the associated risk of overwhelming post-splenectomy infection (OPSI). Current therapeutic approaches prioritize hemostasis and spleen preservation. Prognosis depends on timely diagnosis and adequate management. Therefore, clinicians must maintain high vigilance for patients presenting with unexplained acute abdominal pain accompanied by hemodynamic instability. This article reports a pediatric case of spontaneous splenic rupture and reviews the literature to summarize the pathophysiology, clinical features, and management strategies for this condition.
1 Introduction
Splenic rupture is an uncommon condition. Given the spleen's highly vascular nature, splenic hemorrhage carries significant mortality, particularly when diagnosis is delayed—potentially leading to catastrophic outcomes (1). Spontaneous splenic rupture can be classified into traumatic and atraumatic types. Splenic hemorrhage is most commonly caused by blunt injury, while the incidence of atraumatic splenic rupture is significantly lower (2). Atraumatic splenic rupture, also known as spontaneous splenic rupture (SSR), is a rare but potentially life-threatening condition typically associated with underlying pathological conditions, including neoplasms, hematologic disorders, and inflammatory processes. These pathological states induce splenomegaly and tissue friability, creating the foundation for rupture (1–4). Splenic rupture may still occur in normal spleens, though its incidence is relatively low. Since it is unrelated to any underlying pathology, this condition is termed idiopathic splenic rupture (5, 6).
Given the spleen's critical role in host defense, the primary therapeutic objectives are hemostasis and splenic preservation. However, when patients develop hemodynamic instability accompanied by uncontrolled rupture or recurrent splenic hemorrhage, surgical intervention should be considered the first-line treatment (7, 8). Early identification through diagnostic tools such as computed tomography (CT) and ultrasonography is crucial for improving patient outcomes. The presence of hemoperitoneum is highly suggestive of the diagnosis, and imaging modalities like abdominal CT or ultrasound further aid in confirmation (9–11).
We report a case of SSR in a child. In light of the paramount importance of timely diagnosis and appropriate surgical management in such cases, we will focus on discussing the diagnostic challenges and required surgical approaches for managing SSR. Aiming to describe the clinical characteristics of pediatric splenic rupture, summarize treatment approaches and outcomes, and provide a literature review on this rare condition.
2 Case report
A 6-year-old female patient visited our hospital due to sudden abdominal pain for 1 day. The patient has no history of trauma. Upon admission, the child appeared lethargic. Vital signs include: blood pressure 110/75 mmHg, axillary temperature 36.7 °C, heart rate 106 beats per minute, respiratory rate 26 breaths per minute, and weight 20 kg. Physical examination revealed deep tenderness in the right upper quadrant and right periumbilical area of the abdomen. The abdominal muscles were slightly tense, but there was no rebound tenderness. Laboratory findings showed a Complete Blood Count (CBC) with a White Blood Cell (WBC) count of 6.2 × 10⁹/L, a Red Blood Cell (RBC) count of 3.9 × 10¹²/L, Hemoglobin (Hb) of 114 g/L, Platelets (Plt) of 227 × 10⁹/L, Hematocrit of 35%, Neutrophils at 66.1%, and Lymphocytes at 25.7%. Color Doppler Ultrasound demonstrated no abnormalities in the liver, gallbladder, pancreas, spleen, kidneys, mesenteric vessels, bowel, bilateral ovaries, or uterus; however, an anechoic fluid collection was visualized within the abdominal cavity, with a maximum anteroposterior diameter of approximately 6.4 cm.
Following hospitalization, the decision was made to perform an ultrasound-guided abdominal paracentesis for diagnostic analysis of the fluid. Approximately 20 mL of non-clotting blood was drained. Despite rapid fluid resuscitation, the patient remained hemodynamically unstable. The rechecked blood pressure was 96/60 mmHg. Repeat CBC revealed a RBC count of 2.9 × 10¹²/L, Hb of 89 g/L, and hematocrit of 25%. Given the critical clinical deterioration and absence of a definitive diagnosis, an emergency diagnostic laparoscopy was performed.
An arc-shaped incision was made above the umbilicus to establish a pneumoperitoneum. Upon entering the abdominal cavity with a laparoscope, diffuse hemoperitoneum with significant pelvic blood accumulation, totaling approximately 350 mL. Two 5 mm tissue grasping forceps were inserted at the left subcostal midclavicular line and 2 cm to the right of the umbilicus to assist in exploration. A hematoma was identified between the spleen and liver in the left upper quadrant, anterior to the gastrosplenic ligament. After evacuation of the hematoma, a 2 cm longitudinal laceration was visualized on the superior pole of the spleen near the visceral peritoneal surface, with active pulsatile bleeding. Hemostasis was achieved by packing absorbable hemostatic gauze and applying local omental compression. No rebleeding was observed during a 30 min monitoring period. The incision was then closed. Estimated intraoperative blood loss from the laceration was 250 mL. Transfusion included 100 mL of Fresh Frozen Plasma (FFP) and 3 units of Packed Red Blood Cells (PRBCs). Postoperative repeat CBC showed: RBC count 3.2 × 10¹²/L, Hb 98 g/L, hematocrit 28%. The patient was given tranexamic acid injection (100 mg intravenously, b.i.d.) for 5 days and azithromycin (200 mg intravenously, q.d.) for 3 days. The patient maintained hemodynamic stability with no evidence of rebleeding. Pre-discharge CBC revealed: RBC 3.6 × 10¹²/L, Hb 101 g/L, hematocrit 31%.
This pediatric patient underwent a two year follow-up, remaining clinically well and asymptomatic throughout the period.
3 Discussion
Spontaneous rupture of a histologically normal spleen is an exceedingly rare phenomenon, distinct from traumatic splenic rupture, which involves identifiable physical injury (12, 13). This entity occurs without discernible precipitating factors or underlying pathology, posing significant diagnostic and therapeutic challenges that frequently lead to delayed recognition and management.
The pathophysiological mechanisms underlying spontaneous rupture of histologically normal spleens remain elusive. Several theoretical frameworks have been proposed (13–15): Congenital or acquired vascular abnormalities may predispose the spleen to spontaneous rupture. Microaneurysms or arteriovenous malformations can compromise the integrity of the splenic parenchyma. In susceptible individuals, minor and often unrecognized microtrauma from activities such as heavy lifting or violent coughing may contribute to splenic rupture. Conditions causing abrupt elevation of intra-abdominal pressure—including emesis or strenuous exertion—can precipitate rupture in otherwise healthy spleens. Cases without an identifiable etiology are classified as idiopathic SSR.
SSR predominantly occurs in patients with underlying disorders, particularly hematologic malignancies, infectious diseases, or systemic inflammatory processes (2–4, 13). Etiologic pathogens include but are not limited to Epstein–Barr virus (EBV), hepatitis viruses, Salmonella typhi, Rickettsia prowazekii (typhus), bacterial endocarditis pathogens, Mycobacterium tuberculosis, Brucella spp., Treponema pallidum (syphilis), and cytomegalovirus (CMV) (2, 3, 7, 14). Notably, infectious mononucleosis (IM) secondary to EBV represents the most prevalent infectious cause of SSR (16).
Timely diagnosis of SSR is pivotal for successful management. Diagnostic challenges necessitate integration of physical examination, laboratory findings, and imaging studies. Vital signs may reveal tachycardia and hypotension secondary to hypovolemic shock. Physical signs include: abdominal tenderness, splenomegaly, diminished or absent bowel sounds, Kehr's sign, Ballance's sign, and abdominal guarding (involuntary muscle rigidity) (2, 17–21). Abdominal pain most frequently localizes to the left upper quadrant, though it may manifest in any abdominal quadrant. The pain exhibits variable characterization, ranging from sharp/stabbing to cramping/colicky in nature (1, 15, 21). Kehr's sign manifests as severe discomfort in the scapular or acromial region—predominantly the left shoulder—elicited by the passive leg-raising maneuver in supine position, resulting from diaphragmatic irritation by intraperitoneal blood or other irritants (19). Ballance's sign is characterized by dullness on percussion over the left flank (particularly the left costal region) due to perisplenic hematoma accumulation, with concomitant tympany in the right anterior abdominal wall (20). The absence of trauma history often leads to misdiagnosis as other acute conditions, including acute appendicitis, gastrointestinal perforation, ruptured diverticular abscess, ectopic pregnancy, aortic dissection, myocardial infarction, or pulmonary embolism (13, 22). Laboratory studies typically reveal anemia, characterized by an acute hemoglobin drop of >20 g/L within 24 h (14).
Imaging studies constitute a critical modality for diagnosing splenic rupture, with contrast-enhanced CT (CECT) serving as the preferred initial investigation (10, 11, 13, 14, 21). CECT differentiates etiological factors such as pancreatic body/tail enlargement and splenic flexure tumors, and reveals critical findings—including massive free intraperitoneal fluid and isolated subcapsular hematomas—that directly inform surgical or nonoperative management decisions. Liu et al. (10) recommend CECT for all hemodynamically stable patients with suspected SSR. However, given its portability, rapid acquisition, high sensitivity for solid organ injuries and hemoperitoneum, and absence of ionizing radiation, ultrasonography (US) remains the first-line imaging modality for pediatric populations or hemodynamically unstable patients (13, 23, 24). Furthermore, for unexplained peritoneal effusion, abdominal paracentesis is a quick, convenient, and safe diagnostic method to rapidly clarify the nature of the fluid (25, 26). In this case, the initial US indicated the presence of abdominal effusion without suggesting injury to abdominal organs, leading to the decision to perform an abdominal puncture first to clarify the nature of the effusion. The puncture revealed non-coagulable blood, and due to the child's hemodynamic instability, CECT was not chosen; instead, an emergency laparoscopic exploration was performed.
Magnetic resonance imaging (MRI) has been investigated as a diagnostic tool for visceral injuries, including splenic rupture. It demonstrates exceptional sensitivity for detecting minimal intraparenchymal hemorrhage, subtle capsular tears, and associated soft-tissue injuries. However, its utility in acute settings is constrained by prolonged acquisition times, stringent patient stability requirements, and reduced accessibility compared to CT. Consequently, MRI is typically reserved for follow-up evaluations or specific clinical scenarios necessitating advanced tissue characterization capabilities (13, 14).
The management spectrum for SSR encompasses conservative observation with intensive monitoring, bed rest, splenic artery embolization, splenorrhaphy (including techniques such as Gelfoam packing, omental patching, capsular suturing, or absorbable mesh application), and splenectomy (5, 8, 13, 27). Treatment selection hinges upon the patient's hemodynamic stability and severity of splenic injury, typically graded using the American Association for the Surgery of Trauma (AAST) scale (28). Injuries graded I-III are classified as mild to moderate and are typically amenable to nonoperative management. Conversely, grade IV-V injuries represent high-grade lesions carrying significant mortality risk and generally necessitate surgical intervention. In our case, the child had a splenic capsular tear with a depth of <1 cm, corresponding to a Grade I injury according to the AAST classification, but presented with hemodynamic instability. Therefore, hemostasis was achieved using absorbable hemostatic gauze packing. In our case, the child had a splenic capsular tear with a depth of <1 cm, corresponding to a Grade I injury according to the AAST classification, but presented with hemodynamic instability. Therefore, hemostasis was achieved using absorbable hemostatic gauze packing.
Recent studies advocate nonoperative management as first-line therapy for splenic rupture hemorrhage to mitigate overwhelming post-splenectomy infection (OPSI) risk, particularly critical in pediatric patients who face substantially higher post-splenectomy sepsis vulnerability (5, 8, 27–30). Surgical decision-making should be expedited in hemodynamically unstable patients. When operative management is indicated, spleen-preserving techniques—including surgical suturing combined with absorbable gelatin sponges, mesh, or tissue adhesives—should be prioritized to retain immunologic function (27, 30). When the above treatment plans fail to control bleeding, splenectomy should be performed without delay (22, 31). Overwhelming post-splenectomy infection (OPSI or PSS) is a complication following splenectomy, most commonly caused by Gram-positive encapsulated bacteria. OPSI is primarily caused by Streptococcus pneumoniae, with less common pathogens including Haemophilus influenzae, Neisseria meningitidis, and Gram-negative bacilli. Currently, there are highly effective strategies to prevent infections in post-splenectomy patients, including vaccination, prophylactic antibiotic use (which should be continued for 3 years in children and adolescents), and immediate initiation of antibiotic treatment upon suspected infection. Patients should be educated about the nature and risks of PSS and seek immediate medical attention when ill or febrile. Through these measures and precautions, the risk of PSS can be significantly reduced or even completely avoided (32, 33).
The prognosis of SSR hinges on the timeliness of diagnosis and therapeutic adequacy. Prompt intervention is critical for outcome optimization (8, 13, 27). Therefore, clinicians should enhance their recognition of this condition.
4 Conclusion
Although spontaneous rupture of a histologically normal spleen is rare, it constitutes a critical emergency. Its underlying pathophysiology remains incompletely elucidated, mandating further research. Clinicians must maintain a high index of suspicion for this entity in patients presenting with unexplained acute abdominal pain and hemodynamic instability to ensure expeditious diagnosis and intervention.
Data availability statement
The original contributions presented in the study are included in the article/Supplementary Material, further inquiries can be directed to the corresponding authors.
Ethics statement
Written informed consent was obtained from the individual(s), and minor(s)' legal guardian/next of kin, for the publication of any potentially identifiable images or data included in this article.
Author contributions
XL: Writing – review & editing, Writing – original draft, Software, Methodology, Conceptualization, Validation, Data curation, Investigation. TF: Conceptualization, Methodology, Writing – review & editing, Writing – original draft, Supervision. DL: Writing – original draft, Supervision, Writing – review & editing, Software. GL: Writing – original draft, Software, Writing – review & editing, Supervision. SS: Writing – review & editing, Writing – original draft.
Funding
The author(s) declared that financial support was not received for this work and/or its publication.
Acknowledgments
We thank the colleagues of the Department of Pediatric Surgery and Department of Radiology for their cooperation as well as the enthusiastic support from the operating room team.
Conflict of interest
The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Generative AI statement
The author(s) declared that generative AI was not used in the creation of this manuscript.
Any alternative text (alt text) provided alongside figures in this article has been generated by Frontiers with the support of artificial intelligence and reasonable efforts have been made to ensure accuracy, including review by the authors wherever possible. If you identify any issues, please contact us.
Publisher's note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
References
1. Lieberman ME, Levitt MA. Spontaneous rupture of the spleen: a case report and literature review. Am J Emerg Med. (1989) 7(1):28–31. doi: 10.1016/0735-6757(89)90079-x
2. Ibrahim K, Chalhoub M, Rida M, Smayra T. Sudden abdominal pain in a patient with pneumonia reveals spontaneous splenic rupture in normal sized spleen. Radiol Case Rep. (2024) 19(12):6255–8. doi: 10.1016/j.radcr.2024.08.128
3. Guy S, De Clercq S. Splenic rupture in community acquired pneumonia: a case report. Int J Surg Case Rep. (2016) 29:85–7. doi: 10.1016/j.ijscr.2016.10.054
4. Gedik E, Girgin S, Aldemir M, Keles C, Tuncer MC, Aktas A, et al. Non-traumatic splenic rupture: report of seven cases and review of the literature. World J Gastroenterol. (2008) 14(43):6711–6. doi: 10.3748/wjg.14.6711
5. Renzulli P, Hostettler A, Schoepfer AM, Gloor B, Candinas D. Systematic review of atraumatic splenic rupture. Br J Surg. (2009) 96(10):1114–21. doi: 10.1002/bjs.6737
6. Elvy A, Harbach L, Bhangu A. Atraumatic splenic rupture: a 6-year case series. Eur J Emerg Med. (2011) 18(2):124–6. doi: 10.1097/MEJ.0b013e32833ddeb5
7. Maria V, Saad AM, Fardellas I. Spontaneous spleen rupture in a teenager: an uncommon cause of acute abdomen. Case Rep Med. (2013) 2013:675372. doi: 10.1155/2013/675372
8. Chang HP, Fu RH, Lin JJ, Chiang MC. Prognostic factors and clinical features of neonatal splenic rupture/hemorrhage: two cases reports and literature review. Front Pediatr. (2021) 9:616247. doi: 10.3389/fped.2021.616247
9. Munzi G, Mariolo JR, Poillucci G, Iodice A, Rossi L, Serao A, et al. A spontaneous splenic rupture secondary to epstein barr virus infection: a case report. Int J Surg Case Rep. (2025) 133:111609. doi: 10.1016/j.ijscr.2025.111609
10. Liu J, Feng Y, Li A, Liu C, Li F. Diagnosis and treatment of atraumatic splenic rupture: experience of 8 cases. Gastroenterol Res Pract. (2019) 2019:5827694. doi: 10.1155/2019/5827694
11. Clancy AA, Tiruta C, Ashman D, Ball CG, Kirkpatrick AW. The song remains the same although the instruments are changing: complications following selective non-operative management of blunt spleen trauma: a retrospective review of patients at a level I trauma centre from 1996 to 2007. J Trauma Manag Outcomes. (2012) 6(1):4. doi: 10.1186/1752-2897-6-4
12. Zenaidi H, Ismail IB, Rebii S, Zoghlami A. Predictors of failure of nonoperative management in spleen trauma. J Emerg Trauma Shock. (2020) 13(4):319–20. doi: 10.4103/JETS.JETS_60_20
13. Ismail IB, Sghaier M, Zaafouri EB, Rebii S, Helal I, Jouini R, et al. Spontaneous rupture of a normal spleen: a case report and a review of the literature emphasizing diagnostic and surgical challenges. Int J Surg Case Rep. (2024) 123:110179. doi: 10.1016/j.ijscr.2024.110179
14. Abu Laban AMB, Muhammad W. Spontaneous splenic rupture following severe cough in a patient with community-acquired pneumonia: a case report. Cureus. (2025) 17(5):e85010. doi: 10.7759/cureus.85010
15. Domingo P, Rodriguez P, Lopez-Contreras J, Rebasa P, Mota S, Matias-Guiu X. Spontaneous rupture of the spleen associated with pneumonia. Eur J Clin Microbiol Infect Dis. (1996) 15(9):733–6. doi: 10.1007/BF01691960
16. Baker CR, Kona S. Spontaneous splenic rupture in a patient with infectious mononucleosis. BMJ Case Rep. (2019) 12(9):e230259. doi: 10.1136/bcr-2019-230259
17. Reyes-Jaimes L, Camacho-Aguilera JF. Spontaneous splenic rupture. Case report and literature review. Rev Med Inst Mex Seguro Soc. (2023) 61(4):523–31. doi: 10.5281/zenodo.8200591
18. Eltahir EA, Ibnouf MA, Ibnouf MM, Ahmed MH, Imam MH, Ahmed A. The clinical range and management of spontaneous rupture of the pathological malarial spleen (SRPMS): a short case series from Sudan. Int J Surg Case Rep. (2025) 127:110818. doi: 10.1016/j.ijscr.2025.110818
19. Lowenfels AB. Kehr's sign–a neglected aid in rupture of the spleen. N Engl J Med. (1966) 274(18):1019. doi: 10.1056/NEJM196605052741810
20. Jones LE. Spontaneous rupture of apparently normal spleen. Br Med J. (1944) 2(4373):561–2. doi: 10.1136/bmj.2.4373.561
21. Darnell H, Bidarian S, Brenner A, Auer J. A real gut punch: an unexpected diagnosis of spontaneous splenic rupture. ACG Case Rep J. (2024) 11(7):e01441. doi: 10.14309/crj.0000000000001441
22. Tiboni S, Abdulmajid U, Pooboni S, Wighton C, Eradi B, Dagash H. Spontaneous splenic hemorrhage in the newborn. European J Pediatr Surg Rep. (2015) 3(2):71–3. doi: 10.1055/s-0035-1564610
23. Janez J. Spontaneous splenic rupture 1 week after laparoscopic appendectomy due to acute appendicitis. J Minim Access Surg. (2020) 16(3):269–70. doi: 10.4103/jmas.JMAS_1_20
24. Schwartz K, Krishnasarma R, Snyder E, Pruthi S, Johnstone L, Foust A, et al. Spontaneous splenic rupture in a neonate: a case report and literature review. Emerg Radiol. (2024) 31(1):117–22. doi: 10.1007/s10140-024-02199-0
25. Harvey JJ, Prentice R, George J. Diagnostic and therapeutic abdominal paracentesis. Med J Aust. (2023) 218(1):18–21. doi: 10.5694/mja2.51795
26. Walters JM. Abdominal paracentesis and diagnostic peritoneal lavage. Clin Tech Small Anim Pract. (2003) 18(1):32–8. doi: 10.1016/1096-2867(03)90023-5
27. Hui CM, Tsui KY. Splenic rupture in a newborn. J Pediatr Surg. (2002) 37(4):E3. doi: 10.1053/jpsu.2002.31641
28. Morell-Hofert D, Primavesi F, Fodor M, Gassner E, Kranebitter V, Braunwarth E, et al. Validation of the revised 2018 AAST-OIS classification and the CT severity index for prediction of operative management and survival in patients with blunt spleen and liver injuries. Eur Radiol. (2020) 30(12):6570–81. doi: 10.1007/s00330-020-07061-8
29. Jansen NA, Dittrich A, Backes M, Kusters B, Klein WM, Hundscheid T. Neonatal cardiorespiratory failure caused by splenic hemorrhages: a case report on a fatal and a rescued case. BMC Pediatr. (2024) 24(1):564. doi: 10.1186/s12887-024-05002-8
30. Descamps CS, Cneude F, Hays S, Rayet I, Piolat C, Epiard C, et al. Early hypovolemic shock and abdominal distention due to neonatal splenic rupture: urgency of diagnosis and management. Eur J Pediatr. (2017) 176(9):1245–50. doi: 10.1007/s00431-017-2968-y
31. Adamu I, Asarian A, Xiao P. Splenic rupture and intracranial haemorrhage in a haemophilic neonate: case report and literature review. Afr J Paediatr Surg. (2012) 9(2):163–5. doi: 10.4103/0189-6725.99408
32. Engelhardt M, Haas PS, Theilacker C, Eber SW, Schmugge M, Kern WV, et al. Prävention von infektionen und thrombosen nach splenektomie oder bei funktionsverlust der milz [prevention of infections and thromboses after splenectomy or because of functional loss of the spleen]. Dtsch Med Wochenschr. (2009) 134(17):897–902. doi: 10.1055/s-0029-1220231
Keywords: atraumatic splenic rupture, pediatric surgery, splenic rupture, spontaneous splenic rupture, surgery
Citation: Liu X, Fu T, Li D, Geng L and Sun S (2026) Spontaneous splenic rupture: a case report and literature review. Front. Surg. 12:1687868. doi: 10.3389/fsurg.2025.1687868
Received: 18 August 2025; Revised: 8 December 2025;
Accepted: 10 December 2025;
Published: 5 January 2026.
Edited by:
Nikolaos Zavras, University General Hospital Attikon, GreeceReviewed by:
Mohammadreza Mobayen, Gilan University of Medical Sciences, IranUfuk Akın, Bandirma Onyedi Eylul University, Türkiye
Copyright: © 2026 Liu, Fu, Li, Geng and Sun. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Lei Geng, MzgxODExNDFAcXEuY29t; Shuai Sun, ZHJzdW5zaHVhaTkyQDE2My5jb20=