Prenatal ultrasound diagnosis of a rare morgagni hernia: a case report

Abstract

Background

Morgagni hernia is a rare type of congenital diaphragmatic hernia, and its prenatal diagnosis by ultrasound is extremely challenging, especially when combined with massive pericardial effusion, as it can be easily confused with other diaphragmatic hernias. This article reports a case of fetal Morgagni hernia definitively diagnosed by serial prenatal ultrasound and magnetic resonance imaging, followed by successful intrauterine pericardial drainage and postnatal surgical correction. It aims to emphasize the importance of standardized imaging follow-up for prenatal identification and perinatal management of this condition.

Case presentation

A 28-year-old primigravida with no family history of genetic disorders underwent prenatal ultrasound at an outside hospital at 22 weeks of gestation, which revealed massive fetal pleural effusion, borderline normal width of the left lateral ventricle, and growth parameters below the 2.5th percentile for gestational age. At 27 weeks of gestation, she was referred to our hospital. Ultrasound and magnetic resonance imaging demonstrated a retrosternal liver herniation (Morgagni hernia) accompanied by massive pericardial effusion (range 48 mm × 28 mm). The lungs were compressed, but the lung-to-head ratio was 1.53, indicating acceptable lung development. After family consent, successful intrauterine pericardial drainage was performed at an outside hospital, with significant improvement in lung expansion observed 4 weeks post-procedure. A male infant weighing 2400 g was delivered by cesarean section at 39⁺ weeks of gestation. Postnatal imaging confirmed the Morgagni hernia, and on the second day after birth, diaphragmatic herniorrhaphy was performed, during which the herniated liver was reduced and the diaphragmatic defect was sutured. The infant recovered well after surgery.

Conclusion

This case demonstrates the value of serial prenatal ultrasound combined with magnetic resonance imaging for the accurate diagnosis of Morgagni hernia with pericardial effusion. It also confirms that intrauterine pericardial drainage, when lung development is acceptable, can effectively relieve fetal lung compression and create favorable conditions for postnatal surgical correction, reflecting the positive impact of integrated prenatal–postnatal management on the prognosis of this rare diaphragmatic hernia.

Morgagni hernia, also known as retrosternal hernia, is a rare type of congenital diaphragmatic hernia (CDH), accounting for approximately 3%–5% of all CDH cases [1]. Its anatomical basis lies in the incomplete closure of the sternocostal triangle (Morgagni foramen) during diaphragmatic embryonic development—a potential weak area between the sternal and costal fibers of the diaphragm located on either side of the sternum—resulting in a defect through which abdominal viscera protrude into the thoracic cavity. As the anterior portion of the left diaphragm is reinforced by pericardial fibers, the left sternocostal triangle is relatively robust; consequently, this hernia occurs predominantly on the right side [2]. Accurate prenatal ultrasound diagnosis is crucial for the perinatal management and prognostic evaluation of this condition. This study presents a retrospective analysis of a fetal case prenatally diagnosed with right-sided Morgagni hernia, aiming to provide a reference for the prenatal diagnosis, perinatal management, and surgical treatment of Morgagni hernia.

Case presentation

The pregnant woman was a 28-year-old female with no prior family history of genetic disorders, and physical examination and laboratory tests revealed no significant abnormalities. At 22 weeks of gestation, she underwent a prenatal ultrasound examination at an outside hospital. The ultrasound findings were as follows: the fetal cranial ring was intact, the midline was centrally located, the cavum septi pellucidi was visible, and the bilateral anterior horns of the lateral ventricles were abducted and dilated, presenting a “cow horn” appearance. The width of the posterior horn of the left lateral ventricle was approximately 9.3 mm, and both thalami were visible. The biparietal diameter was 57 mm, head circumference 206 mm, abdominal circumference 178 mm, femoral length 38 mm, and humeral length 37 mm. The transverse cerebellar diameter was 25 mm, and the cisterna magna width was approximately 7.5 mm. The placenta was located on the posterior wall, grade 0, with a thickness of 21 mm. The maximum amniotic fluid pocket depth was 59 mm, and the amniotic fluid index was 174 mm. A singleton fetus was present with a discernible fetal position, good fetal movement, and a fetal heart rate of 154 beats per minute. Focused examination of the thoracic cavity showed that the heart was mostly located in the left hemithorax with the cardiac apex pointing toward the left anterior direction (Fig. 1A). The bilateral thoracic cavities were symmetrical, and a large amount of anechoic fluid was observed filling the thoracic cavities. Both lungs were compressed and reduced in size, with the right lung area measuring approximately 11.7 mm × 8.2 mm (Fig. 1B). Ultrasound findings suggested: ① massive fetal pleural effusion; ② borderline normal width of the left lateral ventricle; ③ fetal head circumference and femoral length both below the M-2SD line for gestational age.

Fig. 1.

Prenatal two-dimensional ultrasound images at 22 weeks of gestation (A-B). A Transverse section of the fetal chest shows a large amount of fluid in the thoracic cavity (P). B Transverse section of the fetal chest shows the lungs (white triangles) compressed and displaced posteriorly within the thoracic cavity. (H: heart; P: pleural effusion)

At 27 weeks of gestation, the pregnant woman was referred to our hospital for further evaluation due to a finding of massive pleural effusion on an ultrasound examination performed at an outside hospital. She underwent only one prenatal ultrasound examination at our hospital, which revealed the following: the fetus was in cephalic presentation; biparietal diameter was 70 mm, head circumference 236 mm, left lateral ventricle width approximately 8.3 mm, right lateral ventricle width 8.3 mm, and cisterna magna width approximately 11 mm; abdominal circumference was 205 mm, and femoral diameter 47 mm. The placenta was located on the posterior wall, grade I maturity, with a thickness of 21 mm. The maximum amniotic fluid pocket depth was 79 mm, and the amniotic fluid index was 266 mm, with good internal echogenicity. Focused examination of the thoracic cavity: two-dimensional ultrasound in the transverse section of the chest showed a large amount of effusion around the fetal heart, measuring approximately 48 mm × 28 mm. Both lungs were compressed and displaced posteriorly, reduced in size and adherent to the posterior chest wall; the right lung measured approximately 19 mm × 11 mm, and the left lung approximately 17 mm × 9 mm (Fig. 2A). The lung-to-head ratio calculated using a head circumference of 236 mm was 1.53, indicating acceptable lung development. In the sagittal plane of the chest, a retrosternal isoechoic mass measuring approximately 20 mm × 10 mm was observed, with echogenicity similar to that of liver parenchyma (Fig. 2B). Three-dimensional ultrasound in both transverse and sagittal planes more stereoscopically demonstrated that the blood supply of this mass originated from the intrahepatic portal vein (Fig. 2C), confirming that part of the liver tissue had herniated into the thoracic cavity through a diaphragmatic defect (Fig. 2D). Based on the above findings, the ultrasound diagnosis was as follows: ① abnormal fetal liver position and an intrathoracic isoechoic mass, suggestive of Morgagni hernia with massive pericardial effusion; ② reduced lung volume; ③ borderline normal width of the bilateral lateral ventricles and widened cisterna magna; ④ fetal head circumference and femur below the M-2SD line; ⑤ polyhydramnios. Prenatal fetal pelvic magnetic resonance imaging further showed mild dilation of the bilateral lateral ventricles, and a portion of the liver (asterisk) herniated into the pericardial sac filled with effusion within the thoracic cavity (Fig. 3A); the coronal image showed a large amount of effusion around the fetal heart (Fig. 3B). In view of the massive pericardial effusion in this fetus, but with a lung-to-head ratio indicating acceptable lung development and a relatively favorable prognostic basis, the family consented to successful intrauterine pericardial drainage performed at an outside hospital. Four weeks after the procedure, local follow-up examination showed significant improvement in lung expansion, with satisfactory results. The plan was to undergo corrective surgery after birth.

Fig. 2.

Prenatal two-dimensional and three-dimensional ultrasound images at 27 weeks of gestation (A-D). A Axial view of the fetal chest shows a large amount of fluid surrounding the heart (H), indicative of pericardial effusion (P). The lungs (white triangles) are compressed and displaced posteriorly within the thoracic cavity. B Sagittal view of the fetal chest demonstrates a portion of the liver (L, asterisk) herniating into the thoracic cavity through a diaphragmatic defect, extending into the pericardial space, with abundant pericardial effusion (P). C Axial view of the fetal chest demonstrates hepatic vessels (white arrows) extending from the abdomen into the thoracic cavity, confirming liver herniation through a diaphragmatic defect. The right lung (white triangle) is compressed and displaced posteriorly. D Sagittal view reveals a solid mass (asterisk) posterior to the sternum (St).(H: heart; P: pericardial effusion; L: liver; *: the herniated liver tissue; Sp: spine; St: Sternum)

Fig. 3.

Prenatal MRI images (A-B). A Sagittal image shows part of the intra-abdominal liver (L, asterisk) herniating into the fluid-filled pericardial cavity (P). B Coronal image shows a large amount of effusion (P) around the fetal heart (H). (P: pericardial effusion; L: liver; *: herniated liver tissue; H: heart )

The mother delivered a male infant weighing 2400 g by cesarean section at 39⁺ weeks of gestation at another institution, with Apgar scores of 9 at 1 min and 10 at 5 min. On the day of birth, the neonate was transferred to our NICU and received conventional mechanical ventilation via endotracheal intubation (settings: PIP 15 cmH₂O, PEEP 5 cmH₂O, respiratory rate 30 breaths/min, FiO₂ 30%). Preoperative ultrasound, X-ray, and chest CT were performed at our hospital. Ultrasound examination revealed partial liver tissue herniating into the thoracic cavity through a diaphragmatic defect on both longitudinal (Fig. 4A) and transverse (Fig. 4B) retrosternal views, with the herniated liver located anterior and to the right of the heart, causing mild cardiac compression. No significant fluid accumulation was observed in the thoracic or pericardial cavities. A median sagittal view of the anterior chest wall further confirmed discontinuity of the diaphragm anterior to the heart, with a portion of the liver displaced superiorly and positioned anterior to the heart (Fig. 4C). Axial chest CT demonstrated intact bony structures of the thorax, clearly visible aerated lung tissue in both thoracic cavities, and a soft tissue mass in the precordial region composed of the heart, thickened pericardium, and herniated liver (Fig. 5A). Sagittal CT further revealed an enlarged cardiac silhouette in the precordial area, partial liver herniation into the thoracic cavity through the diaphragmatic defect, mild mediastinal shift, and slight compression of both lungs (Fig. 5B). Chest and abdominal X-ray also showed enlargement of the cardiac silhouette due to superior displacement of the herniated liver tissue and mild compression of both lungs (Fig. 5C). CT and X-ray findings corroborated each other, clearly confirming the presence of herniated liver tissue and indicating that, although both lungs remained mildly compressed, they were well-aerated with no obvious signs of pulmonary hypoplasia, suggesting improved postnatal lung development compared with the prenatal assessment. Collectively, these preoperative imaging findings demonstrated the typical anatomical features of Morgagni hernia, providing reliable anatomical evidence for subsequent surgical correction.

Fig. 4.

Postnatal two-dimensional ultrasound images (A–C). A Longitudinal view posterior to the sternum shows partial liver tissue herniating into the thoracic cavity through a diaphragmatic defect, with the herniated liver located anterior and to the right of the heart. B Transverse view demonstrates the herniated liver anterior and to the right of the heart, with mild cardiac compression. C Median sagittal view of the anterior chest wall reveals a slightly elevated liver position anterior to the heart, with a portion of the right liver lobe adjacent to the heart.(H: heart; L: liver)

Fig. 5.

Postnatal CT and X-ray images (A-C). A Axial chest CT image shows a soft tissue mass in the precordial region, composed of the heart, thickened pericardium, and herniated liver. B Sagittal CT image reveals an enlarged cardiac silhouette in the precordial area, mild mediastinal shift, and slight compression of both lungs. C Chest and abdominal X-ray demonstrates an enlarged cardiac silhouette and compression of the bilateral lung fields

On the second day after birth, the infant underwent open surgical repair of the right diaphragmatic hernia. Intraoperatively, a portion of the right liver lobe was observed herniating into the right thoracic cavity through an approximately 20 mm × 20 mm defect in the anteromedial aspect of the right diaphragm, with a hernia sac present. A markedly enlarged pericardium was identified posterior to the sternum, and no significant fluid accumulation was found upon opening the pericardial cavity. The hernia sac was partially composed of pericardium and was densely adherent to the superior aspect of the right liver lobe. The adhesions were carefully dissected, and the herniated liver was reduced. The diaphragmatic defect was closed by suturing, and the pericardial cavity and surgical incision were closed in layers. The surgical procedure was uneventful. The intraoperative findings further confirmed the diagnosis of Morgagni hernia in this infant. Postoperatively, mechanical ventilation was continued, and the neonate’s respiratory status gradually improved. Subsequent follow-up indicated favorable recovery.

Discussion

Prenatal ultrasound examination is the primary modality for the early diagnosis of Morgagni hernia. In this case, the outside hospital at 22 weeks of gestation misinterpreted massive pericardial effusion as “pleural effusion” and failed to identify the existing Morgagni hernia. In fact, the pericardial effusion was caused by partial liver herniation through a diaphragmatic defect into the retrosternal space, compressing the pericardium. The outside hospital did not recognize the herniated contents nor correctly identify the pericardial origin of the effusion. Possible reasons include: the large pericardial effusion caused cardiac and mediastinal displacement and poor visualization of the retrosternal region, together with failure to routinely examine the sagittal plane or use Doppler to trace blood supply, thereby missing the herniated liver tissue. As gestational age increased, intra-abdominal pressure rose further, and the herniated liver increased in size. At 27 weeks of gestation, our hospital’s ultrasound accurately identified the liver herniation and massive pericardial effusion (range 48 mm × 28 mm) using two‑dimensional transverse and sagittal planes, and measured the lung-to-head ratio (LHR) as 1.53 to assess lung development. Furthermore, combined three‑dimensional ultrasound and power Doppler stereoscopically demonstrated that the blood supply of the mass originated from the intrahepatic portal vein, confirming it as liver tissue and effectively differentiating it from mediastinal tumors or other space‑occupying lesions. The combined use of two‑dimensional and three‑dimensional ultrasound not only improved diagnostic accuracy but also provided important imaging evidence for evaluating the nature, extent, and degree of compression of the herniated contents. Prenatal MRI served as a complementary modality, displaying the extent of liver herniation and pericardial effusion in multiple planes and with a large field of view [3]; in this case it also confirmed liver herniation into the pericardial sac, corroborating the ultrasound findings. Postnatal imaging is equally indispensable in preoperative assessment: ultrasound can dynamically observe the relationship between the herniated liver, heart, and pericardium, and assess the resolution of effusion [4]; CT, with its high spatial resolution, clearly demonstrates the thoracic bony structures, pulmonary aeration, and mediastinal shift, precisely revealing the soft-tissue mass composed of the herniated liver, heart, and thickened pericardium [5]; X-ray globally shows cardiomegaly and lung compression. The mutual confirmation among multiple imaging modalities not only defined the anatomical features of Morgagni hernia but also indicated that postnatal lung development was improved compared with the prenatal status, providing a reliable basis for surgical timing and procedure design.

Once the diagnosis of Morgagni hernia is established, it is crucial to distinguish pericardial effusion from pleural effusion, which requires detailed analysis of the direction of lung displacement. In pericardial effusion, fluid accumulates within the pericardial cavity and compresses the lung tissue primarily laterally and posteriorly, causing bilateral lungs to shift posteriorly and adhere to the posterior chest wall; lung volume is reduced but the interlobar fissures remain preserved. In pleural effusion, fluid is freely distributed within the pleural space and exerts centripetal compression on the lungs, pushing them toward the hilum. This manifests as inward retraction of the lung parenchyma with blunted margins, and the effusion may be extensive enough to envelop the pulmonary lobes. In the present case of Morgagni hernia with massive pericardial effusion, ultrasound showed compressed and posteriorly displaced lungs adherent to the posterior chest wall, which is consistent with the pattern of lung displacement seen in pericardial effusion. In contrast, simple massive pleural effusion typically results in lungs being compressed toward the hilum, presenting as “floating lung” or centripetal collapse. Therefore, careful observation of the direction of lung displacement (posterior displacement vs. hilar retraction), together with signs such as diaphragmatic defect, retrosternal liver herniation, and portal venous blood supply, can effectively distinguish Morgagni hernia‑associated pericardial effusion from pleural effusion or mixed effusion due to other causes, thereby avoiding misdiagnosis. Further exploration of the pathogenesis of Morgagni hernia with massive pericardial effusion suggests two hypotheses based on existing research [6]. First, hepatic venous outflow obstruction: the herniated liver tissue in the thoracic cavity compresses the hepatic veins or the inferior vena cava, leading to venous return impairment, which in turn causes hepatic congestion and exudation of fluid into the pericardial cavity via the diaphragmatic defect or lymphatic channels. Second, thoracic duct compression: the herniated contents may compress the thoracic duct, obstructing normal lymphatic return and resulting in abnormal accumulation of lymph fluid within the pericardial cavity. Although the massive pericardial effusion in this case compressed both lungs posteriorly and increased the risk of pulmonary hypoplasia, the fetus did not exhibit cardiac dysfunction or signs of cardiac tamponade. This may be attributed to slow accumulation of the effusion and gradual compensatory dilatation of the pericardium, which provided a favorable window for intrauterine intervention and postnatal surgical treatment.

Based on the mechanistic analysis above, the prognosis of this condition is primarily determined by the developmental status of the lungs and heart [7]. In this case, the fetal lung-to-head ratio (LHR) measured at 27 weeks of gestation by prenatal ultrasound was 1.53. This parameter, calculated as the ratio of the contralateral lung area to the head circumference, is a crucial quantitative indicator for assessing the degree of fetal lung development and predicting the prognosis of congenital diaphragmatic hernia [8]. The value of 1.53 suggested acceptable lung development and a favorable prognostic foundation, providing key evidence for clinical decision-making. Consequently, the family successfully underwent intrauterine pericardiocentesis at another institution. This intervention effectively alleviated the compression on the lung tissue, and follow-up at four weeks post-procedure showed marked improvement in lung expansion, creating favorable conditions for postnatal surgical correction. Postnatal imaging examinations revealed that although both lungs remained mildly compressed, they were well-aerated with no obvious signs of pulmonary hypoplasia, indicating further improvement in lung development compared with the prenatal period. Open diaphragmatic hernia repair was performed on the second day after birth, and the intraoperative findings were consistent with the prenatal diagnosis. Of note, intraoperative observation revealed a thickened pericardium with dense adhesions to the superior aspect of the right liver lobe. This may be attributed to the following factors: long-term stimulation by pericardial effusion leading to fibrous tissue proliferation and inflammatory response in the parietal pericardium, resulting in thickening and adhesions; concurrently, prolonged contact and friction between the herniated liver and the pericardial wall may have induced localized reactive thickening. The infant’s respiratory status gradually improved after surgery, and follow-up indicated favorable recovery. The clinical course described above further underscores the core value of prenatal ultrasound in perinatal management: by assessing the degree of lung development through quantitative parameters such as LHR, it provides a basis for decision-making regarding intrauterine intervention.

The pathogenesis and development of congenital diaphragmatic hernia (CDH) are closely related to genetic factors. Previous studies have shown that various copy number variations and gene sequence variants, particularly those involving genes of the retinoic acid signaling pathway, play a key role in the pathogenesis of this malformation [9]. However, the embryonic development of the diaphragm involves complex events such as cell migration, cytoskeletal remodeling, and myogenesis, suggesting that the candidate gene spectrum for CDH extends far beyond the retinoic acid signaling pathway and may encompass a broader genetic regulatory network. Regarding genetic evaluation, the fetus in this case presented with multiple major abnormalities including diaphragmatic hernia and pericardial effusion, which constitute clear indications for prenatal genetic testing. The pregnant woman underwent amniocentesis at an outside hospital, and chromosomal microarray analysis (CMA) and fluorescence in situ hybridization (FISH) were performed; all results were normal. Therefore, no definite pathogenic copy number variants were identified at the genetic level.

The prenatal ultrasound differential diagnosis of Morgagni hernia hinges on establishing a systematic evaluative approach, which necessitates consideration from three dimensions: anatomical location, tissue origin, and secondary changes, while comprehensively accounting for various conditions that may present as an intrathoracic mass, mediastinal shift, or pericardial effusion. Specifically, in the differential diagnosis among congenital diaphragmatic hernias, Morgagni hernia is characteristically located in the retrosternal anteromedial region, frequently accompanied by a hernia sac, with the herniated liver receiving blood supply from the portal venous system. In contrast, Bochdalek hernia is typically situated in the posterolateral aspect of the thorax, often with a large defect and usually without a hernia sac [10]. Hiatal hernia manifests as a cystic structure protruding above the diaphragm, potentially displaying gastric mucosal folds or air-fluid levels, and maintains continuity with the infradiaphragmatic stomach. Pulmonary sequestration commonly presents as a mixed solid-cystic lesion in the posterior basal segment of the lower lobe, with three-dimensional ultrasound enabling the tracing of its anomalous systemic arterial blood supply [11]. Furthermore, differentiation from diaphragmatic abnormalities such as eventration or diaphragmatic dysplasia is required; these conditions are characterized by an intact but attenuated and elevated diaphragm, lacking a distinct diaphragmatic defect and the portal venous supply feature of herniated liver tissue [12]. Regarding the differential diagnosis of mediastinal shift, it is essential to determine whether the displacement is secondary to an intrathoracic mass or pulmonary hypoplasia. Mediastinal shift caused by Morgagni hernia is typically accompanied by a clearly identifiable intrathoracic hepatic mass and interruption of diaphragmatic continuity, whereas primary mediastinal lesions, such as intrathoracic cystadenomatoid malformation or bronchogenic cysts, exhibit heterogeneous internal echotexture with mixed solid and cystic components, and color Doppler imaging typically reveals blood supply originating from the systemic circulation [13]. In the context of pericardial effusion differentiation, the effusion in Morgagni hernia is closely related to the position of the herniated liver, with the liver tissue observed adjacent to the pericardium. In comparison, primary pericardial diseases lack evidence of liver herniation and diaphragmatic defects, while pericardial effusion secondary to heart failure can be identified by echocardiography demonstrating underlying cardiac structural abnormalities [14]. Therefore, echocardiography plays a critical role in evaluating cardiac structure and the characteristics of pericardial fluid; combined with three-dimensional ultrasound for visualizing the blood supply of the herniated liver tissue, it effectively distinguishes Morgagni hernia from pericardial effusion due to other etiologies.

This case report has several limitations. First, the prenatal imaging data are incomplete. The fetus underwent only two ultrasound examinations: one at an outside hospital (22 weeks of gestation) and one at our hospital (27 weeks of gestation), precluding continuous dynamic observation at more frequent time points. Moreover, the ultrasound records provided by the outside hospital at 22 weeks lacked specific measurements of the left lung area and the exact effusion volume, and the outside hospital declined to provide the ultrasound images taken after the pregnant woman underwent intrauterine pericardial drainage, preventing an objective imaging comparison to assess the degree of lung expansion improvement following the intrauterine intervention. Second, although genetic evaluation was not entirely absent (the pregnant woman underwent amniocentesis at an outside hospital with chromosomal microarray analysis and fluorescence in situ hybridization, both showing no definitive pathogenic copy number variants), higher‑resolution testing such as whole‑exome or whole‑genome sequencing was not performed. Therefore, the possibility of monogenic disorders or non‑coding region variants cannot be completely excluded, and parental validation analysis was not conducted, limiting in-depth exploration of the genetic background of this disease. Furthermore, as a single case report, the sample size is limited, and the generalizability of the conclusions requires validation with more cases. Although pericardial thickening and adhesions were observed intraoperatively, no tissue was obtained for pathological examination, preventing a definitive pathological characterization of the pericardial lesions. Finally, long-term follow-up data are incomplete; there is a lack of long-term assessment of the child’s growth and development, cardiopulmonary function, and quality of life, precluding a comprehensive evaluation of the long‑term prognosis of this disease. Future efforts should accumulate more case data, improve high‑resolution genetic testing, and establish long‑term follow-up to further deepen the understanding of Morgagni hernia complicated by pericardial effusion.

In summary, this case systematically demonstrates the full-course management of Morgagni hernia, from prenatal diagnosis and intrauterine intervention to postnatal evaluation and surgical repair. Prenatal ultrasound served as the primary diagnostic modality, identifying the diaphragmatic defect and secondary changes such as pericardial effusion via two‑dimensional ultrasound, and combined with three‑dimensional ultrasound and power Doppler to precisely trace the portal venous blood supply of the herniated liver, thereby achieving an accurate qualitative diagnosis of Morgagni hernia. Measurement of the lung‑to‑head ratio provided a key quantitative basis for assessing lung development and predicting prognosis. Successful intrauterine pericardial drainage effectively relieved lung compression and created favorable conditions for postnatal lung improvement. Postnatal multimodal imaging (ultrasound, CT, and X‑ray) corroborated each other, not only clarifying the anatomical relationship between the herniated liver, heart, and thickened pericardium, but also confirming continued improvement in postnatal lung development. Intraoperative observation of pericardial thickening and adhesions, possibly related to long‑term effusion irritation and mechanical friction, provided intuitive evidence for understanding the pathophysiological process of the disease. In terms of differential diagnosis, a systematic evaluation approach based on three dimensions – anatomical location, tissue origin, and secondary changes – can effectively distinguish Morgagni hernia from other congenital diaphragmatic hernias, pulmonary sequestration, diaphragmatic abnormalities, as well as primary and secondary pericardial effusions. Although genetic evaluation in this case (chromosomal microarray analysis and fluorescence in situ hybridization) revealed no definite pathogenic copy number variants, higher‑resolution whole‑exome or whole‑genome sequencing was not performed, and long‑term follow‑up data are lacking, representing certain limitations. Nevertheless, the complete diagnostic and treatment course fully reflects the core value of multimodal imaging in the precise diagnosis, perinatal management, and individualized treatment of Morgagni hernia, providing a useful reference for the management of similar clinical cases.

Abbreviations

CDH

Congenital Diaphragmatic Hernia

LHR

Lung-to-Head Ratio

CT

Computed Tomography

CMA

Chromosomal Microarray Analysis

FISH

Fluorescence In Situ Hybridization

L

Liver

H

Heart

MRI

Magnetic Resonance Imaging

P

Pericardial Effusion

FiO₂

Fraction of Inspired Oxygen

NICU

Neonatal Intensive Care Unit

PEEP

Positive End-Expiratory Pressure

PIP

Peak Inspiratory Pressure

RA

Retinoic Acid

Sp

Spine

St

Sternum

Author contributions

1. Conception and design: T Pan, T Li; (II) Administrative support: B Ma, T Li; (III) Provision of study materials or patients: B Ma; (IV) Collection and assembly of data: T Pan, T Li, W Pang, G Wang; (V) Manuscript writing: All authors; (VI) Final approval of manuscript: All authors.

Funding

This study was supported by the Outstanding Talent Program (Grant No. GMCCH2025-2-2-02).

Data availability

not applicable.

Declarations

Ethics approval and consent to participate

All procedures performed in this study were in accordance with the ethical standards of the Medical Ethics Committee of Gansu Provincial Maternity and Child-Care Hospital and with the Helsinki Declaration (as revised in 2013). Written informed consent was obtained from the patient’s next of kin for publication of this article and any accompanying images.

Competing interests

The authors declare no competing interests.