Chronic liver disease (CLD) in children refers to persistent hepatic injury or dysfunction lasting for several months and encompassing a broad spectrum of disorders that may progress from inflammation and fibrosis to cirrhosis and portal hypertension.1,2 Unlike adults, in whom alcohol-related and metabolic liver diseases are prominent, pediatric CLD has a heterogeneous etiology that includes viral hepatitis, genetic and metabolic disorders, autoimmune liver disease, congenital biliary abnormalities, and increasingly metabolic dysfunction-associated steatotic liver disease (MASLD).3,4  The World Health Organization estimated that 0.6% of children younger than five years were living with chronic hepatitis B infection globally in 2024, despite a substantial decline from the pre-vaccine era.5 Metabolic liver disease is also becoming increasingly relevant in childhood; a recent global analysis estimated MASLD prevalence at approximately 7.0% among individuals aged 5–24 years.6

Regardless of the initiating cause, prolonged hepatic injury promotes inflammatory responses, activation of hepatic stellate cells, and progressive deposition of extracellular matrix within the liver. Fibrotic remodeling gradually distorts normal hepatic architecture and may culminate in cirrhosis.7 Increasing intrahepatic vascular resistance subsequently contributes to portal hypertension, which can produce splenic congestion, enlargement, and alterations in splenic tissue characteristics. Thus, structural and hemodynamic changes occur not only within the liver but also in the spleen as CLD advances.8

Liver stiffness and splenic stiffness are therefore important measurable manifestations of chronic hepatic injury and portal hypertensive change. Liver stiffness primarily reflects the mechanical properties of hepatic tissue, which increase with fibrosis but may also be influenced by inflammation and other transient factors.9 Splenic stiffness reflects changes associated with portal hypertension and altered splenic architecture and vascular congestion. Assessment of both parameters can provide complementary information regarding hepatic fibrosis and the extrahepatic consequences of chronic liver disease.10

Shear wave elastography (SWE) is an ultrasound-based technique that quantifies tissue stiffness by generating mechanical shear waves and measuring their propagation through tissue. It can be incorporated into conventional ultrasonography, permits real-time localization of the measurement region, and avoids the need for a separate mechanical pulse-generating device.11 In children, SWE-derived liver stiffness has demonstrated variable thresholds across studies, with reported fibrosis-related cut-offs approximately ranging from 1.24 to 1.89 m/s; measurements may also increase in the presence of hepatic inflammation. By applying the same non-invasive elastographic principle to the liver and spleen, SWE enables quantitative assessment of tissue stiffness without biopsy and allows these two related manifestations of pediatric chronic liver disease to be evaluated within the same imaging examination.12,13

Chronic liver disease in children causes progressive hepatic fibrosis and portal hypertensive changes, making non-invasive assessment of liver and splenic stiffness clinically relevant. Although recent Pakistani evidence has demonstrated a significant correlation between liver stiffness measured by SWE and biopsy-proven fibrosis, local data assessing both hepatic and splenic stiffness together in pediatric CLD remain limited. Therefore, this study will provide local evidence on SWE-derived liver and splenic stiffness and their relationship with chronic liver disease severity, adding pediatric data from Pakistan to the existing international literature.

This was a hospital-based cross-sectional study that was conducted in the Department of Radiology in collaboration with the relevant pediatric unit from January 2026 to June 2026. A total of 120 pediatric patients with chronic liver disease were enrolled. The sample size of 120 patients was calculated using the WHO/OpenEpi sample size formula for estimation of a proportion, taking an expected frequency of the relevant finding from previously published pediatric elastography literature, a 95% confidence level, and an appropriate margin of error. The calculated minimum sample was approximately 120 patients, which was adopted as the final sample size. Published pediatric studies have demonstrated the feasibility of shear wave elastography for quantitative assessment of hepatic stiffness, while more recent work has also evaluated splenic stiffness in children with chronic liver disease. Children aged 1–18 years with a clinical or laboratory diagnosis of chronic liver disease were included. Patients with acute liver disease, acute hepatitis, previous liver transplantation, significant cardiac disease causing hepatic congestion, known splenic pathology unrelated to chronic liver disease, or inability to cooperate adequately during ultrasonographic examination were excluded. Children with conditions that could substantially alter tissue stiffness independently of chronic liver disease were also excluded. Written informed consent was obtained from the parents or legal guardians, while assent was obtained from children where appropriate. Ethical approval was obtained from the institutional review committee before commencement of the study. Demographic and clinical information was recorded, including age, sex, relevant cause of chronic liver disease, duration of disease, and clinical evidence of chronic liver dysfunction or portal hypertension. Relevant laboratory investigations, including liver function tests and platelet count, were recorded when available. Routine abdominal ultrasonography was performed before elastography to assess liver and spleen size, hepatic echotexture, focal abnormalities, biliary tract changes, and other associated findings. Shear wave elastography (SWE) was performed using a conventional ultrasound machine equipped with a two-dimensional SWE module and an appropriate convex transducer. Patients were examined in the supine position after fasting for approximately four hours. The liver was examined through a right intercostal acoustic window during quiet respiration. The transducer was applied with minimal pressure, and the region of interest was placed within the right hepatic lobe while avoiding large vessels, bile ducts, and areas of artifact. Multiple measurements were obtained from different acquisitions, and the mean liver stiffness value was recorded in kPa and/or m/s. Similar pediatric SWE protocols have used multiple measurements and standardized probe positioning to improve measurement reliability. Splenic stiffness was subsequently measured using the same SWE system. The spleen was visualized through an appropriate intercostal or subcostal window, and the region of interest was positioned within homogeneous splenic parenchyma while avoiding vessels and the splenic capsule. Multiple valid measurements were obtained during quiet respiration, and the mean value was recorded as the splenic stiffness. Pediatric studies have demonstrated the feasibility of obtaining repeated spleen stiffness measurements using ultrasound elastography. The primary outcome variables were liver stiffness and splenic stiffness measured by SWE. The recorded elastography values were compared according to relevant clinical and laboratory characteristics, including the presence or absence of features suggestive of advanced chronic liver disease or portal hypertension. Data were entered into and analyzed using SPSS. Continuous variables were expressed as mean ± standard deviation or median with interquartile range according to data distribution, whereas categorical variables were expressed as frequencies and percentages. Appropriate comparative tests were applied for continuous and categorical variables, and a p-value <0.05 was considered statistically significant.

The study included 120 children with chronic liver disease, with a mean age of 10.2 ± 4.1 years. The participants were predominantly male, and the mean duration of chronic liver disease was 3.8 ± 2.6 years. The largest proportion belonged to the 11–15-year age group, followed by children aged 6–10 years, as shown in Table 1.

Table 1. Demographic characteristics of children with chronic liver disease (n=120)

Viral hepatitis was the most frequent etiology of chronic liver disease, followed by autoimmune hepatitis and Wilson disease. Biliary disorders and metabolic liver disease accounted for smaller proportions, while cryptogenic or other causes constituted the remaining cases, as given in Table 2.

Table 2. Etiological distribution of chronic liver disease among the study patients (n=120)

Among the clinical findings, splenomegaly was the most frequently observed feature, followed by hepatomegaly. Clinical jaundice was present in approximately one-third of the patients, whereas ascites was documented in a smaller proportion, as shown in Table 3.

Table 3. Clinical characteristics of children with chronic liver disease (n=120)

Shear wave elastography demonstrated measurable stiffness in both the liver and spleen, with the mean splenic stiffness being higher than the corresponding liver stiffness when expressed in kPa. The recorded values showed variability among the study participants, as given in Table 4.

Table 4. Liver and splenic stiffness measurements by shear wave elastography (n=120)

Children with splenomegaly had higher mean liver stiffness and splenic stiffness measurements than those without splenomegaly. The differences in both elastography parameters were statistically significant, with p-values below 0.001, as shown in Table 5.

Table 5. Comparison of liver and splenic stiffness according to splenomegaly (n=120)

A statistically significant positive correlation was observed between liver stiffness and splenic stiffness, indicating that higher liver stiffness measurements were associated with higher splenic stiffness measurements among the studied children, as given in Table 6.

Table 6. Correlation between liver and splenic stiffness measurements (n=120)

Chronic liver disease in children is a heterogeneous condition caused by viral, autoimmune, metabolic, genetic, and biliary disorders and may progress to hepatic fibrosis, cirrhosis, and portal hypertension. Progressive fibrosis alters the mechanical properties of hepatic tissue, while portal hypertension can produce splenic congestion and increased splenic stiffness.14 Liver and splenic stiffness therefore represent important measurable features of chronic liver disease. Shear wave elastography is a non-invasive ultrasound-based technique that quantitatively measures tissue stiffness and can be performed during routine abdominal ultrasonography.15 Assessment of both liver and splenic stiffness may provide complementary information about hepatic and splenic involvement in pediatric chronic liver disease. This study assessed these elastographic parameters in children with chronic liver disease. In the present study, shear wave elastography demonstrated measurable hepatic and splenic stiffness in 120 children with chronic liver disease, with mean liver stiffness of 10.84 ± 5.21 kPa and mean splenic stiffness of 28.72 ± 12.46 kPa. A significant positive correlation was observed between liver and splenic stiffness (r=0.58, p<0.001), while children with splenomegaly had significantly higher liver stiffness (12.72 ± 5.48 vs. 8.89 ± 3.91 kPa, p<0.001) and splenic stiffness (34.86 ± 11.74 vs. 22.36 ± 8.42 kPa, p<0.001). These findings were broadly consistent with the pediatric elastography literature, although differences in disease etiology, severity, elastography technique, and outcome definitions resulted in variation in absolute stiffness values. Özkan et al. (2018) evaluated 56 children with biopsy-proven liver disease and 38 healthy controls and successfully obtained reliable liver stiffness measurements in 85% (80/94) and splenic stiffness measurements in 81% (76/94) of participants. Splenic stiffness was significantly higher in children with portal hypertension (p<0.01). Their diagnostic analysis demonstrated an AUC of 0.906 for liver p-SWE compared with 0.746 for splenic p-SWE (p=0.0239); a liver stiffness cut-off of 2.09 m/s provided 77.27% sensitivity and 80.28% specificity, whereas a splenic stiffness cut-off of 3.14 m/s yielded 68.18% sensitivity and 98.59% specificity. The present study similarly demonstrated higher stiffness values in children with evidence of splenic involvement, supporting the association between elastographic measurements and manifestations of portal hypertensive disease, although direct comparison of absolute values was limited because the present study reported stiffness predominantly in kPa and did not use the same diagnostic cut-offs.16 Imtiaz et al. (2025) evaluated the correlation between shear wave elastography and liver biopsy in 37 children with chronic liver disease from Pakistan. The mean age was 10 years (range 4–14 years), and autoimmune hepatitis was the most common etiology, accounting for 43% of cases. The overall mean liver stiffness was 12.14 ± 0.75 kPa. Liver stiffness increased progressively with histological fibrosis, measuring 6.00 ± 0.01 kPa in F0–F1, 7.67 ± 0.29 kPa in F2, 8.62 ± 0.20 kPa in F3, and 14.05 ± 3.69 kPa in F4 (p=0.0001). In the present study, the mean liver stiffness was 10.84 ± 5.21 kPa, which was comparable to the overall value reported by Imtiaz et al. (12.14 ± 0.75 kPa). The progressive increase in liver stiffness across fibrosis stages in their study was also consistent with the elevated stiffness observed in the present cohort, although histological fibrosis staging was not performed in our study. Importantly, Imtiaz et al. provided evidence from the Pakistani pediatric population, whereas the present study additionally assessed splenic stiffness, with a mean value of 28.72 ± 12.46 kPa, and demonstrated a significant positive correlation between liver and splenic stiffness (r=0.58, p<0.001).17 Yuldashev et al. (2020) further demonstrated the relationship between splenic stiffness and portal hypertensive changes in children. Their study showed that children in group A had a mean esophageal variceal grade of 2.3 ± 0.14 (p<0.001), which was significantly higher than in groups B and C, while surgical shunting in group C reduced the variceal grade to 0.37 ± 0.14. Mean splenic stiffness was 70.0 ± 4.64 kPa in group A, 37.04 ± 4.62 kPa in group B, and 26.3 ± 2.9 kPa in group C, with a significant difference among the groups (p<0.001). Following surgery, splenic stiffness decreased but remained significantly higher than that of controls (26.3 ± 2.9 vs. 17.85 ± 1.3 kPa, p=0.016). Splenic stiffness also showed a significant correlation with esophageal variceal grade (r=0.56, p=0.002).18 More recently, Geng et al. (2026) assessed 40 children with biliary atresia and 45 controls and found that both liver stiffness values (LSV) and spleen stiffness values (SSV) were significantly higher in the biliary atresia group (p<0.001). SSV showed significant associations with spleen size, splenic vein diameter, and platelet count (all p<0.01), while multivariate analysis identified splenic vein velocity as an independent predictor of SSV and total bilirubin as a significant influence on LSV (p<0.05). For prediction of surrogate portal hypertension, SSV produced an AUC of 0.78 (95% CI: 0.63–0.93), compared with 0.76 (95% CI: 0.61–0.90) for LSV. These findings were compatible with the present observation that splenic stiffness was substantially elevated in children with splenomegaly and that hepatic and splenic stiffness were significantly correlated.19 Chaurasia et al. (2025) reported that both hepatic and splenic stiffness were higher in children with chronic liver disease than in controls, and that stiffness values were further increased among children with CLD and portal hypertension. The difference in splenic elastography measurements between children with CLD with and without portal hypertension was statistically significant. This pattern closely paralleled the present findings, particularly the significantly higher splenic stiffness among children with splenomegaly (34.86 ± 11.74 vs. 22.36 ± 8.42 kPa, p<0.001). The concordance was particularly relevant because splenomegaly represents an important clinical manifestation of portal hypertensive involvement. However, the present study additionally demonstrated a significant direct relationship between hepatic and splenic stiffness, with r=0.58 (p<0.001), providing a quantitative association between the two principal elastographic outcomes.20 Overall, the findings across these studies consistently demonstrated that hepatic and splenic stiffness measurements obtained by elastography were associated with the severity or manifestations of chronic liver disease and portal hypertensive changes in children, while the present study further demonstrated a significant relationship between the two stiffness parameters themselves. STUDY LIMITATIONS The study was conducted at a single center, which may limit the generalizability of the findings to the wider pediatric population. The cross-sectional design did not allow assessment of changes in stiffness measurements over time. Liver biopsy was not performed for histological correlation with elastography findings. Variations in the etiology and stage of chronic liver disease may also have influenced stiffness measurements.

Shear wave elastography demonstrated increased liver and splenic stiffness among children with chronic liver disease, particularly in those with splenomegaly. Liver stiffness and splenic stiffness showed a significant positive correlation. These findings support the use of SWE as a non-invasive method for simultaneous assessment of hepatic and splenic stiffness in pediatric chronic liver disease.

Acknowledgement: We sincerely acknowledge the support and guidance of our mentors, colleagues, and the staff of the participating hospital for their valuable assistance throughout this study.

Conflict of Interest: No

Funding Disclosure: None

1. Maggiore G, Corte CD, Liccardo D, Mosca A, Pietrobattista A. Children with chronic liver disease. InFrailty in children: From the perioperative management to the multidisciplinary approach 2023 Mar 4 (pp. 69-87). Cham: Springer International Publishing.
2. Suthantirakumar RL, Gupte GL. Timing and indications for liver transplantation for children with chronic liver disease. Children. 2025 Mar 31;12(4):449.
3. Tampaki M, Tsochatzis E, Lekakis V, Cholongitas E. Prevalence, characteristics and outcomes of patients with metabolic and alcohol related/associated liver disease (MetALD): a systematic review and meta-analysis. Metabolism. 2025 Feb 1;163:156101.
4. Åberg F, Jiang ZG, Cortez-Pinto H, Männistö V. Alcohol-associated liver disease-Global epidemiology. Hepatology. 2024 Dec 1;80(6):1307-22.
5. de Villiers MJ, de Villiers E, Nayagam S, Hallett TB. Direct and indirect effects of hepatitis B vaccination in four low-and middle-income countries. Epidemics. 2024 Dec 1;49:100798.
6. Liu Y, Cai S, Yang R, Lin J, Dang J, Huang T, Li J, Zhu K, Chen Z, Zhang Y, Song Y. Global and regional prevalence, burden, and risk factors for MASLD in children and adolescents aged 5 to 24 years: a systematic review, meta-analysis, and modeling study. BMC medicine. 2026 Mar 18;24(1):267.
7. Hammerich L, Tacke F. Hepatic inflammatory responses in liver fibrosis. Nature reviews Gastroenterology & hepatology. 2023 Oct;20(10):633-46.
8. Akkız H, Gieseler RK, Canbay A. Liver fibrosis: from basic science towards clinical progress, focusing on the central role of hepatic stellate cells. International Journal of Molecular Sciences. 2024 Jul 18;25(14):7873.
9. Dajti E, Ravaioli F, Zykus R, Rautou PE, Elkrief L, Grgurevic I, Stefanescu H, Hirooka M, Fraquelli M, Rosselli M, Chang PE. Accuracy of spleen stiffness measurement for the diagnosis of clinically significant portal hypertension in patients with compensated advanced chronic liver disease: a systematic review and individual patient data meta-analysis. The Lancet Gastroenterology & Hepatology. 2023 Sep 1;8(9):816-28.
10. Reiberger T. The value of liver and spleen stiffness for evaluation of portal hypertension in compensated cirrhosis. Hepatology communications. 2022 May;6(5):950-64.
11. Caenen A, Pernot M, Nightingale KR, Voigt JU, Vos HJ, Segers P, D'hooge J. Assessing cardiac stiffness using ultrasound shear wave elastography. Physics in Medicine & Biology. 2022 Jan 21;67(2):02TR01.
12. Ageeli WA. Ultrasound Shear Wave Elastography in Oncology: Principles, Performance, and Clinical Applications: A Review. Saudi Journal of Health Research & Practice. 2026 Jan 30;2(1):32-41.
13. Leong SS, Jalalonmuhali M, Md Shah MN, Ng KH, Vijayananthan A, Hisham R, Wong JH. Ultrasound shear wave elastography for the evaluation of renal pathological changes in adult patients. The British Journal of Radiology. 2023 Apr 1;96(1144):20220288.
14. Zou YG, Wang H, Li WW, Dai DL. Challenges in pediatric inherited/metabolic liver disease: Focus on the disease spectrum, diagnosis and management of relatively common disorders. World Journal of Gastroenterology. 2023 Apr 14;29(14):2114.
15. Ray G. Management of liver diseases: Current perspectives. World journal of gastroenterology. 2022 Oct 28;28(40):5818.
16. Özkan MB, Bilgici MC, Eren E, Caltepe G. Diagnostic accuracy of point shear wave elastography in the detection of portal hypertension in pediatric patients. Diagn Interv Imaging. 2018;99(3):151-156. doi:10.1016/j.diii.2017.10.009.
17. Imtiaz M, Khaqan MU, Mazhar M, Seerat I. Correlation of shear wave elastography with liver biopsy in children with Chronic Liver disease. Pak J Med Sci. 2025;41(2):585-589. doi:10.12669/pjms.41.2.9886.
18. Yuldashev RZ, Aliev MM, Shokhaydarov SI, Tursunova DB. Spleen stiffness measurement as a non-invasive test to evaluate and monitor portal hypertension in children with extrahepatic portal vein obstruction. Pediatric Surgery International. 2020 May;36(5):637-41.
19. Geng C, Tan J, Yan X, Huang S, Fu M, Yuan L. Spleen and liver shear wave elastography for assessment of portal hypertension in children with biliary atresia. Scientific Reports. 2026 Jun 14.
20. Chaurasia D, Batra R, Dixit R, Singh H. 2D shear wave elastography in children with chronic liver disease with & without portal hypertension. Ultrasound in Medicine & Biology. 2025 Jan 1;51:S28.