Multiple Sclerosis During Pregnancy and the Postpartum Period: Diagnostic and Multidisciplinary Challenges in Two Cases

Abstract

Background

Pregnancy may complicate the recognition and evaluation of new neurological symptoms suggestive of a central nervous system demyelinating disease. Diagnostic uncertainty may arise when clinical progression, neuroimaging findings, and supportive investigations are incomplete or inconclusive.

Case Presentation

We report two pregnant women with progressive focal neurological symptoms and radiological findings suggestive of a demyelinating disease. Case 1 involved a 27-year-old woman with a history of autoimmune spondyloarthritis who developed dizziness, gait instability, asymmetric weakness, paraesthesia, and neuropathic pain during pregnancy. She underwent preterm delivery, and postpartum MRI demonstrated juxtacortical hyperintense lesions. Case 2 involved a 24-year-old woman who developed progressive right-sided weakness, visual disturbances, and headache during pregnancy. MRI demonstrated multiple periventricular and subcortical hyperintense lesions. She subsequently experienced spontaneous preterm labor and neurological worsening during the early postpartum period. In both cases, the available clinical and radiological findings raised concern for a demyelinating disorder; however, incomplete diagnostic investigations precluded retrospective confirmation of a definitive multiple sclerosis phenotype.

Conclusion

These two cases highlight the diagnostic and clinical challenges associated with neurological symptoms suggestive of demyelinating disease during pregnancy and the postpartum period. Careful interpretation of clinical and radiological findings, continued postpartum surveillance, individualized obstetric decision-making, and multidisciplinary collaboration are essential. These observations should not be interpreted as evidence of causal relationships between suspected demyelinating disease and adverse obstetric outcomes.

Plain Language Summary

Multiple sclerosis (MS) is a chronic disease affecting the brain and spinal cord that commonly affects women of reproductive age. Pregnancy and the postpartum period may create challenges when new neurological symptoms suggestive of a demyelinating disorder develop. This report describes two pregnant women who experienced progressive neurological symptoms and brain imaging abnormalities that raised concern for a central nervous system demyelinating disease. In one case, symptoms developed early in pregnancy and persisted after delivery. In the other, neurological symptoms worsened during the early postpartum period. However, the available retrospective clinical and diagnostic information was insufficient to confirm a definitive MS phenotype in either patient. These cases highlight the importance of careful neurological assessment, appropriate interpretation of imaging findings, continued postpartum follow-up, and collaboration among obstetricians, neurologists, radiologists, and other specialists when significant neurological symptoms occur during pregnancy.

Introduction

Multiple sclerosis (MS) is a chronic immune-mediated inflammatory and demyelinating disease of the central nervous system that predominantly affects young adults, and is more prevalent among women of reproductive age.¹ Consequently, pregnancy may coincide with the onset, recognition, or ongoing evaluation of neurological symptoms suggestive of central nervous system demyelinating disease.² Clinical manifestations may include motor weakness, sensory disturbances, visual symptoms, impaired coordination, and cranial nerve dysfunction, creating diagnostic challenges when neurological symptoms first develop or worsen during pregnancy.²

Pregnancy and the postpartum period present specific challenges in the assessment of suspected demyelinating disease and in the management of women with established MS. Diagnostic investigations and therapeutic decisions require careful consideration of maternal neurological status, disease severity, and fetal safety.³ Magnetic resonance imaging plays an important role in evaluating central nervous system lesions; however, imaging findings should be interpreted in conjunction with the clinical presentation, temporal evolution of symptoms, and other supportive investigations.⁴ Differential diagnosis is particularly important because several inflammatory, autoimmune, infectious, vascular, and other neurological disorders may mimic MS or present with similar neurological manifestations during pregnancy.⁵

Although the interaction between MS and pregnancy has been widely discussed, individual patients may present with considerable diagnostic uncertainty and require complex and obstetric decision-making.⁶ The following report presents two contrasting cases of pregnant women with progressive neurological symptoms and radiological findings suggestive of demyelinating disease. These cases illustrate the challenges of establishing diagnostic certainty, interpreting evolving neurological findings, and coordinating individualized multidisciplinary management during pregnancy and the early postpartum period.

Case Illustration

Case 1

A 27-year-old woman, gravida 5 para 2 abortus 2, presented to the emergency department during early pregnancy with acute abdominal and lumbosacral pain, dizziness, and a syncopal episode. She estimated her gestational age to be approximately three months, and ultrasonography confirmed a viable intrauterine pregnancy at 13–14 weeks’ gestation. Her medical history included autoimmune spondyloarthritis, for which she had been receiving rheumatologic care since April 2023. Her previous medications included methotrexate, methylprednisolone, and calcium carbonate. After pregnancy was confirmed at eight weeks’ gestation, methotrexate was discontinued and replaced with azathioprine because of its teratogenic potential. Her obstetric history included a preterm stillbirth, two spontaneous abortions, and one surviving child.

During hospitalization, neurological consultation was requested because of dizziness, gait instability, and asymmetric limb symptoms that had progressed over the preceding week. She reported episodic spinning vertigo, intermittent tinnitus, and neuropathic pain radiating from the left shoulder to the arm and from the lower back to the left leg. These symptoms were followed by heaviness and weakness of the left side accompanied by paraesthesia. She denied dysarthria and facial deviation. Neurological examination demonstrated mild central paresis involving cranial nerves VII and XII and asymmetric motor strength (5/4 and 5/3 in selected muscle groups), while cognitive function was preserved (MMSE 24/30). These findings prompted further neurological evaluation for a central nervous system disorder, including an inflammatory or demyelinating process.

At 16 weeks’ gestation, obstetric ultrasonography showed appropriate fetal biometrics without structural abnormalities. The patient continued folic acid (400 µg), iron supplementation, methylprednisolone (6 mg daily), and calcium carbonate. Her nutritional status was suboptimal, with a BMI of 17.1 kg/m². At 19 weeks’ gestation, a follow-up anomaly scan identified a 2.8-mm membranous ventricular septal defect (VSD), and serial fetomaternal monitoring was arranged. Throughout pregnancy, her neurological symptoms persisted, including fluctuating left-sided weakness, recurrent vertigo, and neuropathic pain, requiring continued clinical observation.

At 34–35 weeks’ gestation, preterm delivery was undertaken in the context of worsening maternal neurological symptoms. The preterm neonate had a low birth weight and was admitted to the neonatal intensive care unit because of respiratory distress. Postnatal echocardiography confirmed the previously identified small membranous VSD. The infant subsequently developed hemodynamic instability and died three days after delivery.

Two weeks postpartum, non-contrast brain MRI and MRA were performed as part of further diagnostic evaluation of persistent neurological symptoms (Figure 1). The radiological examination demonstrated mild white matter abnormalities involving the bilateral juxtacortical parietal regions and left temporal regions, with findings considered suggestive of a demyelinating process; multiple sclerosis was included in the radiological differential diagnosis. No evidence of cerebral venous sinus thrombosis or vascular malformation was reported. Cerebrospinal fluid analysis showed a normal opening pressure (180 mmH₂O), clear appearance, mild lymphocytic predominance, normal protein concentration, and a CSF-to-serum glucose ratio of 58%.

Figure 1.

Brain MRI findings in Case 1. Selected coronal (a and b) and axial (c) T2-weighted turbo spin-echo (TSE) brain MRI obtained during neurological evaluation. Mild white matter signal abnormalities are noted as focal hyperintensities involving the bilateral juxtacortical parietal regions and the left temporal region as indicated by the white arrows. These neuroimaging findings are highly suggestive of an inflammatory demyelinating process, with multiple sclerosis being a leading consideration in the differential diagnosis.

Postpartum, the patient experienced partial improvement in paraesthesia and motor function but continued to have residual left-sided weakness and neuropathic pain. She was counselled regarding continued neurological follow-up and further diagnostic evaluation. Her postpartum recovery was otherwise uneventful, without infectious or obstetric complications.

Case 2

A 24-year-old woman, gravida 3 para 1 abortus 1, at approximately 31–32 weeks’ gestation, presented for a routine antenatal visit without obstetric complaints. Obstetric ultrasonography demonstrated a single live cephalic fetus consistent with 32 weeks’ gestation, with an estimated fetal weight of 1920 g (44.9^th percentile), normal amniotic fluid volume, and no detectable structural abnormalities. Doppler velocimetry of the umbilical artery, middle cerebral artery, and uterine arteries were within normal physiological ranges.

During the antenatal assessment, the patient reported progressive right-sided weakness that had developed insidiously earlier in pregnancy. Her symptoms were accompanied by visual disturbances, pain with eye movement, and chronic headaches. Neurological examination revealed right-sided facial paresis and reduced motor strength, while sensory and cognitive functions remained intact. Brain MRI performed during pregnancy demonstrated multiple T2/FLAIR hyperintense lesions in the periventricular and subcortical regions, findings compatible with a possible inflammatory or demyelinating process (Figure 2). The patient had previously been treated with pyridostigmine for suspected myasthenia gravis; however, the medication was discontinued because of intolerance.

Figure 2.

Brain MRI findings in Case 2. Brain MRI in different sections of the brain are shown, sequentially moving superiorly through the periventricular and subcortical white matter (a–d): T2-weighted fluid-attenuated inversion recovery (flair) images. The pictures show several distinct, hyperintense oval plaques in both hemispheres of the brain. Deep periventricular white matter plaque in the right hemisphere and juxtacortical plaque in the left hemisphere (a), superiorly extending into deep subcortical tracts of the frontal white matter (b) and parietal (c and d) white matter (arrows). The overall pattern, bilateral distribution, and distinct morphology are very typical of a central nervous system demyelinating disease like multiple sclerosis.

Her antenatal course was initially uncomplicated. She subsequently developed spontaneous preterm labor, and an emergency caesarean section was performed in the setting of preterm labor and concurrent maternal neurological symptoms. The procedure was completed without intraoperative complications, and both the mother and neonate were initially clinically stable postpartum.

Approximately seven days after delivery, the patient reported further worsening of her neurological deficits, particularly right-sided weakness. This clinical deterioration prompted further neurological assessment. Based on the available clinical presentation, neuroimaging findings, and temporal evolution of symptoms, the neurological findings remained suggestive of a central nervous system demyelinating disorder.

Postpartum treatment included calcium supplementation, vitamin D₃, folic acid, and iron. Continued neurological follow-up and further diagnostic evaluation were planned, with subsequent management individualized according to maternal clinical status and breastfeeding considerations. At reassessment, the patient remained hemodynamically stable and cognitively intact. Cranial nerve examination demonstrated persistent right-sided central facial paresis and mild hypoglossal deficits. Her obstetric recovery was otherwise unremarkable, although neurological symptoms persisted during the early postpartum period. The clinical, neurological, obstetric, and diagnostic characteristics of the two cases are summarized in Table 1, while the major clinical events and postpartum trajectories are presented chronologically in Table 2.

Table 1.

Comparison of Clinical, Neurological, Obstetric, and Diagnostic Characteristics of the Two Cases

Characteristic	Case 1	Case 2
Maternal age (years)	27	24
Obstetric status	G5P2A2	G3P1A1
Gestational age at initial neurological assessment	First/early second trimester	Approximately 31–32 weeks
Relevant comorbidity	Autoimmune spondyloarthritis	None documented
Initial neurological symptoms	Dizziness, vertigo, gait instability, left-sided weakness, paraesthesia, and neuropathic pain	Progressive right-sided weakness, visual disturbances, pain with eye movement, and chronic headache
Neurological examination findings	Mild central paresis involving cranial nerves VII and XII; asymmetric motor weakness	Right-sided facial paresis and reduced motor strength; persistent mild hypoglossal involvement documented postpartum
Previous neurological diagnosis	No documented prior diagnosis of demyelinating disease	Previously diagnosed with suspected myasthenia gravis and treated with pyridostigmine
Previous immunomodulatory treatment	Methotrexate and methylprednisolone before pregnancy; methotrexate discontinued after pregnancy recognition; azathioprine subsequently prescribed	Pyridostigmine previously prescribed for suspected myasthenia gravis and discontinued because of intolerance
MRI timing	Two weeks postpartum	During pregnancy
MRI sequences documented	Non-contrast T2-weighted MRI; detailed sequence/plane information unavailable	T2/FLAIR imaging reported; detailed plane and contrast information unavailable
MRI findings	Multiple hyperintense lesions in bilateral juxtacortical parietal regions and left temporal lobe	Multiple T2/FLAIR hyperintense lesions in periventricular and subcortical regions
CSF examination	Opening pressure 180 mmH2O; clear appearance; mild lymphocytic predominance; normal protein concentration; CSF-to-serum glucose ratio 58%	Not available
Oligoclonal bands/IgG index	Not available in retrospective records	Not available
EDSS score	Not available in retrospective records	Not available in retrospective records
Diagnostic interpretation	Clinical and radiological findings suggestive of an inflammatory/demyelinating CNS disorder; definitive MS phenotype could not be retrospectively established	Clinical and radiological findings suggestive of a demyelinating CNS disorder; definitive MS phenotype could not be retrospectively established
Obstetric outcome	Preterm delivery at 34–35 weeks	Spontaneous preterm labor followed by emergency caesarean delivery
Neonatal outcome	Low-birth-weight neonate admitted to NICU for respiratory distress; antenatally detected small membranous VSD; early neonatal death	Neonate initially stable postpartum
Postpartum neurological course	Partial improvement in paraesthesia and motor function with residual left-sided weakness and neuropathic pain	Significant worsening of right-sided neurological deficits approximately 7 days postpartum

Table 2.

Timeline of Clinical Events in Case 1 and Case 2

Timing	Case 1	Case 2
Pre-pregnancy	History of autoimmune spondyloarthritis; previously treated with methotrexate and methylprednisolone	Previous neurological symptoms had been evaluated and treated as suspected myasthenia gravis with pyridostigmine, which was discontinued because of intolerance
Early pregnancy	Pregnancy confirmed at approximately 8 weeks; methotrexate discontinued and azathioprine initiated	Progressive right-sided weakness reportedly developed earlier during pregnancy
13–14 weeks	Presented with acute abdominal and lumbosacral pain, dizziness, syncopal episode, gait instability, asymmetric weakness, paraesthesia, vertigo, and neuropathic pain; neurological consultation obtained	—
16 weeks	Obstetric ultrasonography showed appropriate fetal growth without structural abnormalities	—
19 weeks	Anomaly scan identified a 2.8-mm membranous ventricular septal defect; serial fetomaternal monitoring arranged	—
Mid-to-late pregnancy	Persistent fluctuating left-sided weakness, recurrent vertigo, and neuropathic pain	Progressive right-sided weakness accompanied by visual disturbances, pain with eye movement, and chronic headache
Approximately 31–32 weeks	—	Routine antenatal assessment demonstrated normal fetal growth and Doppler findings; neurological examination showed right-sided facial paresis and reduced motor strength
During pregnancy	No definitive neurological diagnosis established	Brain MRI demonstrated multiple T2/FLAIR hyperintense lesions in periventricular and subcortical regions, suggestive of an inflammatory or demyelinating process
34–35 weeks	Preterm delivery undertaken in the context of worsening maternal neurological symptoms	Spontaneous preterm labor developed subsequently
Delivery	Preterm delivery; neonate admitted to NICU for respiratory distress	Emergency caesarean section performed for preterm labor in the setting of concurrent maternal neurological symptoms
Early postpartum	Partial improvement in paraesthesia and motor function, with persistent residual weakness and neuropathic pain	Approximately 7 days postpartum, worsening of right-sided weakness was reported
2 weeks postpartum	Non-contrast brain MRI demonstrated bilateral juxtacortical parietal and left temporal hyperintense lesions; CSF analysis performed	Continued neurological assessment and follow-up planned
Postpartum follow-up	Continued neurological follow-up and further diagnostic evaluation recommended	Persistent neurological deficits during early postpartum period; continued neurological follow-up and further diagnostic evaluation planned

Discussion

This report describes two pregnant women who developed progressive focal neurological symptoms accompanied by neuroimaging abnormalities suggestive of a central nervous system demyelinating disorder. Although multiple sclerosis (MS) predominantly affects young adults and women of reproductive age, the recognition of new neurological symptoms during pregnancy remains clinically challenging because diagnostic evaluation and management must consider both maternal neurological status and pregnancy-related factors.⁷ The principal value of the present report lies not in establishing a causal relationship between suspected demyelinating disease and adverse obstetric outcomes, but in illustrating the diagnostic uncertainty, differing clinical trajectories, and multidisciplinary challenges that may arise when significant neurological symptoms develop during pregnancy and persist into the postpartum period.⁸

A central challenge in both cases was diagnostic certainty. The diagnosis of MS requires integration of clinical findings, neuroimaging, evidence of dissemination in space and time, and exclusion of alternative diagnoses.^9,10 In these retrospective cases, key diagnostic data were unavailable or incompletely documented, including cerebrospinal fluid oligoclonal bands, IgG index, serial MRI, and comprehensive evaluation for alternative neurological disorders. Although both patients were clinically considered to have a possible demyelinating disorder and MS was suspected, the available evidence was insufficient to establish a definitive diagnosis according to established criteria.^10,11 This distinction is important because focal neurological deficits and white matter abnormalities may occur in inflammatory, autoimmune, vascular, infectious, and other neurological conditions.^9,12 Therefore, alternative diagnoses should remain under consideration when the clinical course or available investigations are insufficient to confirm MS.^10,13

The diagnostic uncertainty was particularly evident in Case 1. The patient developed dizziness, gait instability, asymmetric weakness, paresthesia, and cranial nerve involvement in the context of a pre-existing autoimmune condition. Her neurological symptoms evolved progressively rather than as a clearly documented discrete neurological attack. Postpartum MRI demonstrated hyperintense lesions involving the bilateral juxtacortical parietal regions and left temporal lobe, raising clinical concern for a possible inflammatory or demyelinating process. The juxtacortical distribution of the lesions is recognized as a characteristic MRI pattern in MS and contributes to the assessment of dissemination in space.¹⁴ MRI plays a central role in the assessment of suspected MS; however, lesion location and imaging findings should be interpreted together with clinical presentation and other supportive investigations rather than as isolated confirmation of the diagnosis.¹⁴ In addition, the available cerebrospinal fluid findings were non-specific and did not include oligoclonal band testing or an IgG index. The coexistence of autoimmune spondyloarthritis warranted consideration of alternative immune-mediated disorders in the differential diagnosis.¹⁵ Therefore, the findings in Case 1 support clinical suspicion of a demyelinating process but require cautious interpretation.

Case 2 followed a different diagnostic pathway. Progressive right-sided weakness associated with visual disturbances and pain with eye movement was accompanied by multiple periventricular and subcortical T2/FLAIR hyperintense lesions on MRI performed during pregnancy. Periventricular lesions are among the characteristic locations evaluated during MRI assessment of suspected MS; nevertheless, MRI abnormalities alone are not sufficient to establish the diagnosis without appropriate clinical correlation and exclusion of mimicking disorders.^4,16 The previous diagnosis of myasthenia gravis and treatment with pyridostigmine further illustrate the potential for diagnostic uncertainty when neurological symptoms arise during pregnancy. Taken together, the contrasting presentations of both patients highlight the importance of systematic diagnostic evaluation when progressive neurological symptoms are accompanied by white matter abnormalities, particularly to avoid premature diagnostic closure.¹³

Pregnancy may further complicate the assessment of suspected demyelinating disease because clinicians must balance the need for timely neurological investigation with maternal and fetal considerations.¹⁷ Contemporary reviews emphasize that pregnancy should not preclude appropriate neurological evaluation when clinically indicated, particularly in patients with persistent, progressive, or disabling focal neurological deficits.^18,19 In the present report, the timing of neuroimaging differed according to the clinical circumstances. Case 1 underwent non-contrast MRI postpartum as part of further evaluation of persistent symptoms, whereas Case 2 underwent MRI during pregnancy because of progressive focal deficits. This difference represents an important educational aspect of the report, illustrating that diagnostic strategies should be individualized according to clinical urgency and maternal–fetal considerations.²⁰ Neuroimaging findings should subsequently be interpreted in conjunction with lesion distribution, morphology, clinical evolution, supportive investigations, and relevant differential diagnoses.²¹

The postpartum neurological trajectories also differed between the two patients. Case 1 demonstrated partial improvement in paraesthesia and motor function after delivery, although residual weakness and neuropathic pain persisted. In contrast, Case 2 experienced worsening of right-sided weakness approximately seven days postpartum. Studies involving women with established relapsing MS have demonstrated changes in disease activity during pregnancy and an increased risk of relapse during the early postpartum period.^17,22 Pregnancy-related immunological adaptations have been proposed as contributing to these changes in inflammatory disease activity.¹⁷ However, population-level observations regarding established MS should not be directly applied to individual patients without a firmly established diagnosis and well-documented pre-pregnancy disease course.²³ In Case 2, postpartum deterioration was temporally compatible with neurological worsening after delivery. It may alternatively represent continuation or progression of an ongoing neurological process.²⁴ Similarly, the partial postpartum improvement observed in Case 1 cannot be attributed to a specific pregnancy-related immunological mechanism. Nevertheless, the differing postpartum courses emphasize the importance of continued neurological surveillance after delivery when neurological deficits persist or worsen.^18,25

The obstetric management of both patients was influenced by the coexistence of maternal neurological and pregnancy-related concerns. Case 1 underwent preterm delivery in the setting of worsening maternal neurological symptoms, whereas Case 2 subsequently developed spontaneous preterm labor followed by emergency caesarean delivery. Current evidence suggests that women with established MS can generally experience successful pregnancies, although management should be individualized according to maternal disease status and obstetric circumstances.²⁵ Importantly, the temporal association observed in these two cases should not be interpreted as evidence that suspected demyelinating disease directly caused preterm birth. Similarly, the ventricular septal defect and subsequent early neonatal death in Case 1 cannot be attributed to maternal neurological disease based on the available information. Rather than demonstrating a causal relationship between neurological disease and obstetric outcomes, these cases illustrate the complexity of clinical decision-making when significant maternal neurological symptoms coexist with pregnancy complications. Decisions regarding the timing and mode of delivery should therefore be individualized according to maternal neurological status, obstetric indications, fetal condition, gestational age, and available multidisciplinary expertise.²⁶

A major educational message from both cases is the importance of multidisciplinary collaboration throughout pregnancy and the postpartum period. The management of women with established or suspected demyelinating disease may require coordination between obstetricians and neurologists, with additional involvement of radiologists and neonatologists when clinically indicated.^19,27 In the present cases, neurological assessment and obstetric management occurred simultaneously, and the differing clinical trajectories required individualized decisions regarding imaging, delivery, and postpartum follow-up. Systematic documentation of neurological symptoms and examination findings, timely consideration of neuroimaging, and careful evaluation of alternative diagnoses are particularly important when progressive focal neurological deficits develop during pregnancy.²⁷ Effective communication between specialties is equally important when maternal neurological deterioration coincides with obstetric complications.¹³

Several limitations should be acknowledged. The retrospective nature of this report resulted in incomplete documentation of detailed neurological examinations, longitudinal follow-up, and investigations relevant to diagnostic classification, including oligoclonal bands, IgG index, serial MRI, and assessment of alternative neurological diagnoses. Incomplete information regarding long-term treatment and disease evolution also limited characterization of the underlying neurological phenotype. Furthermore, the inclusion of only two patients precludes conclusions regarding disease behavior, postpartum relapse patterns, or causal relationships between neurological symptoms and obstetric outcomes. These limitations reinforce the need for cautious interpretation and continued reassessment when complete diagnostic investigations are unavailable.¹³

The principal contribution of these two cases is therefore educational rather than inferential. They demonstrate how pregnancy may complicate the recognition and evaluation of progressive neurological symptoms and how diagnostic uncertainty may persist when complete investigations and longitudinal data are unavailable.⁵ The contrasting timing of neuroimaging and postpartum neurological trajectories further illustrate the need for individualized assessment rather than assumptions based solely on typical patterns of established MS. These cases reinforce the importance of careful diagnostic evaluation, avoidance of premature conclusions, continued postpartum surveillance, and multidisciplinary decision-making when suspected central nervous system demyelinating diseases present during pregnancy and the early postpartum period.²⁶

Conclusion

These two cases illustrate the diagnostic and clinical challenges of progressive neurological symptoms suggestive of a demyelinating disorder during pregnancy and the early postpartum period. The differing clinical presentations and postpartum trajectories highlight the heterogeneity of these clinical presentations and the importance of cautious interpretation of neurological and radiological findings, particularly when complete diagnostic investigations and longitudinal data are unavailable. These observations should not be interpreted as evidence of causal relationships between suspected demyelinating disease and adverse obstetric outcomes. Rather, the cases emphasize the importance of timely neurological assessment, individualized obstetric decision-making, continued postpartum surveillance, and multidisciplinary collaboration.

Funding Statement

The authors received financial support for the publication of this article. The article processing charge was funded by Universitas Padjadjaran through the Indonesian Endowment Fund for Education (LPDP) on behalf of the Indonesian Ministry of Higher Education, Science and Technology and managed under the EQUITY Program (Contract No. 4303/B3/DT.03.08/2025 and 3927/UN6.RKT/HK.07.00/2025).

Data Sharing Statement

All data supporting the findings of this study are included within the article. Additional data is not publicly available due to considerations of patient confidentiality and privacy.

Ethics Statement

Ethical approval was obtained from the Health Research Ethics Committee of Dr. Hasan Sadikin General Hospital (Approval No. AR.02.02/D.XIV.3.4.2/450/2025). Institutional approval from Dr. Hasan Sadikin General Hospital was required and was granted for publication of the case details. Written informed consent for publication of the clinical details and accompanying images was obtained from the patients.

Disclosure

The authors declare no conflicts of interest related to this work.