Squamous cell carcinoma in neglected lumbar myelomeningocele successfully managed by multidisciplinary surgical reconstruction

Abstract

Squamous cell carcinoma (SCC) arising within an untreated myelomeningocele (MMC) represents an exceptionally rare but devastating complication of this common neural tube defect, with only 15 cases documented in English literature prior to this report. We present the 16th documented case of SCC in a neglected lumbar MMC and provide a comprehensive critical appraisal of all 15 previously published cases to elucidate epidemiological patterns, treatment heterogeneity, and critical gaps in standardized management protocols. The current case involves a 19-year-old male with a neglected lumbosacral MMC and hydrocephalus who had received only ventriculoperitoneal shunt placement, without surgical closure of the underlying myelomeningocele defect. Over time, chronic ulcerations and repeated infections lead to malignant transformation. Magnetic resonance imaging revealed an Arnold–Chiari II malformation and an extensive mass infiltrating the spinal cord from T11 to S1. En bloc resection with durotomies and reconstruction using bilateral V-Y advancement flaps with latissimus dorsi muscle advancement achieved a complete oncological excision. Adjuvant locoregional radiotherapy was administered for high-risk patients. At two-year follow-up, the patient remained disease free. This case underscores the importance of early MMC closure and vigilant long-term surveillance in resource-limited settings to prevent Marjolin-type degeneration.

Introduction

Myelomeningocele (MMC) results from incomplete neural tube closure during early embryogenesis and affects approximately 0.5–2 per 1,000 live births worldwide [1]. Prompt postnatal surgical closure is the standard treatment for preventing infection, preserving neurologic function, and avoiding secondary complications [1]. In rare instances of chronic, untreated MMC, persistent ulceration and bacterial colonization can lead to malignant transformation, akin to Marjolin’s ulcer, with only 15 cases of Squamous cell carcinoma (SCC) in MMC reported to date (Table 1) [2–16]. Comprehensive review of 15 previously published cases (1967–2025) reveals key epidemiological patterns: 80% lumbar/lumbosacral location (12/15), 67% with cerebrospinal fluid fistula (CSF) (10/15), and paradoxically, 40% well-differentiated histology yet 55% mortality rate—consistent with aggressive Marjolin biology wherein histologic grade does not predict aggressiveness [2–16]. Arnold–Chiari type II malformation and hydrocephalus are nearly universal in MMC, contributing to complex neurologic and orthopedic sequelae [17, 18]. The absence of a protective epithelium creates a nidus for mechanical trauma and chronic infection, culminating in neoplastic changes [19]. Diagnosis is challenging due to altered tissue architecture and frequent superimposed infections; however, rapid lesion growth, ulceration, foul odor, and necrotic cauliflower-like masses should be suspected. Complete surgical excision with clear margins—including durotomies to prevent tumor seeding—followed by reconstructive plastic surgery and adjuvant radiotherapy constitutes the mainstay of treatment [9, 20, 21]. Herein, we present the 16th reported case of SCC arising in a neglected lumbar MMC, detailing a multidisciplinary approach that resulted in a two-year disease-free outcome. This case was written in accordance with the care checklist.

Table 1.

Literature review of reported cases of squamous cell carcinoma in myelomeningocele from 1967 to 2025

N°	Authors (year)	Age/sex	Site	Margins	Management	Adjuvant treatment	Histopathology	Outcome	CSF
1	Pope & Todorov (1975) [2]	37/M	Cervical	–	Surgical Excision	None	SCC	Uneventful recovery	?
2	Banerjee (1977) [3]	20/F	Thoracolumbar (T12-L1)		Palliative RT (spine/groin)	None	SCC	Died (septicemia/anemia)	–
3	Saksun & Fisher (1978) [4]	25/M	Lumbosacral		Antibiotics+ RT (2400 rads) (Surgery deferred)	None	SCC	Died (meningitis)	Purulent discharge (No fistula reported)
4	Marini et al. (1979) [5]	41/M	Lumbar	–	Excision	Cobalt therapy	SCC with Inguinal lymph node metastasis	Alive (8 mo follow-up)	Yes
5	Van Tintelen et al. (1980) [6]	50/M	Lumbar	–	Excision	None	SCC	Died (pneumonia/renal failure)	?
6	Chadduck & Uthman (1984) [7]	29/F	Lumbar	–	Excision	VP Shunt	SCC (Poorly differentiated)	Alive (Discharged)	Yes (Sealed spontaneously)
7	Duan et al. (2009) [8]	11/M	Lumbosacral	–	Excision + repair	Not reported	SCC (Well-differentiated)	Alive (6 yrs follow-up)	Yes (Serosanguinous discharge)
8	Wani et al. (2016) [9]	60/M	Sacral	–	Excision + RT	Referred to RT	SCC (Well-differentiated)	Alive (1 yr follow–up)	–
9	Erhamamci et al. (2016) [10]	26/F	Lumbosacral		Excisional biopsy	None	SCC (Metastatic)	Metastases (inguinal/axillary)	Yes (Foul discharge)
10	Goyal et al. (2018) [11]	21/M	Lumbar	–	Excision + Repair	RT 50 Gy	SCC (Moderately differentiated)	Alive (8 mo follow-up)	No
11	Kurt-Ozkaya (2019) [12]	22/F	Thoraco-sacral (T12-Sacral)		None (Patient refused surgery)	None (refused all treatment)	SCC (Well-differentiated)	Died (septicemia) 20 days post-admission	Yes (Continuous drainage)
12	Alonso Batanero et al. (2023) [13]	67/M	Sacral		Debridement + Biopsies	None (palliative approach)	SCC (Well-differentiated)	Died on admission (Metastases: bone, lung, liver)	Yes (30 yrs evolution)
13	Pinto et al. (2024) [14]	~40/M	Buttocks/Perineum		Unresectable	Palliative care (refused RT & hemicorporectomy)	SCC (Well-differentiated)	Palliative care	Yes (Internally draining)
14	Ndaro Daniel (2025) [15]	13/M	Lumbar	–	Excision + Repair	None	SCC (well differentiated)	Alive (Healed fully)	Yes (2 mo leakage)
15	Gautam et al. (2025) [16]	26/F	Sacral		Biopsy	Not documented	SCC	Loss of follow up	Foul discharge
16	Our Case	19/M	Lumbo-Sacral	–	Excision + Repair	RT 50 Gy	SCC (well differentiated)	Alive (2 years)	Yes

M: Male; F: Female; SCC: Squamous Cell Carcinoma; RT: Radiotherapy; VP: Ventriculo-peritoneal; mo: Months; yrs: Years; CFS: Cerebro-spinal fistula; - : negative

Clinical presentation

A 19-year-old male of North African descent, the fourth child of non-consanguineous parents, presented with a complex medical history in January 2023.The family history was unremarkable for congenital anomalies and neoplastic diseases. At birth, he was diagnosed with lumbosacral myelomeningocele accompanied by hydrocephalus, for which a ventriculoperitoneal shunt was placed at one year of age. Owing to financial constraints, postnatal surgical closure of the myelomeningocele was not performed.

Patient history revealed recurrent episodes of lumbosacral wound drainage and infected lesion episodes over the 19-year period since initial MMC diagnosis at birth. However, formal systemic antibiotic documentation and culture results were not available in transferred medical records.

Over the preceding three months, the lumbosacral lesion exhibited rapid enlargement and developed ulceration with a foul odor. The patient was admitted to the hospital with an infected lumbosacral wound. Physical examination revealed a 20-cm diameter meningomyelocele located in the posterior midline of the lower lumbar region. The lesion appeared as a cauliflower-like, fleshy mass with a central crater containing a necrotic black slough that was adherent to the underlying tissues. The area emitted a pronounced foul odor (Fig. 1).

Fig. 1.

Patient’s lumbosacral region in the prone position, revealing a massive irregularly shaped fungating lesion over the myelomeningocele site. The surface was uneven and exophytic, with areas of bright red granulation tissue interspersed with yellow–green necrotic slough and purulent exudate. Central regions appeared deeply ulcerated, with black eschar and adherent necrosis. The surrounding skin shows hyperpigmentation and chronic pressure-related changes including early callus formation. Hand-drawn surgical planning markings are visible around the defect margins, outlining the intended resection and flap advancement borders

Clinical examination revealed macrocephaly with an enlarged head circumference, dextroscoliosis, flaccid paraparesis, bilateral talipes equinovarus deformities, and urinary incontinence. Pressure ulcers were also present on both the buttocks.

Neurologically, the patient presented with ASIA Grade B paraplegia: absent motor function in the lower extremities (motor score 0) with preserved perianal sensation and anal tone—favorable prognostic indicators. Upper extremity strength remained intact (5/5). These findings reflected chronic spinal cord compression from both Arnold–Chiari II malformation and MMC mass.

A biopsy of the lesion confirmed a diagnosis of SCC. Magnetic resonance imaging (MRI) demonstrated Arnold-Chiari malformation type II, along with a lumbosacral myelomeningocele extending from thoracic vertebral level 11 to sacral level 1 (Fig. 2). A large subcutaneous mass, measuring 156 × 154 mm, occupied the vertebral bony defect and infiltrated the spinal cord. Whole-body computed tomography, including the cranial, thoracic, abdominal, and pelvic regions, showed no evidence of distant metastases.

Fig. 2.

The MRI imaging demonstrated key features characteristic of squamous cell carcinoma rather than chronic infection: (1) solid heterogeneous soft-tissue mass with intermediate and low-signal intensity areas, consistent with viable tumor and central necrosis rather than simple fluid collection; (2) mass effect and spinal cord infiltration, with the tumor displacing and invading the dorsal spinal cord parenchyma—findings not expected from infection alone; (3) nodular wall thickening and exophytic growth pattern suggesting aggressive neoplastic process rather than inflammatory pseudomass; (4) absence of simple fluid signal within the primary lesion, distinguishing this from CSF-containing meningocele or purely infectious abscess. BA (left): Axial T2-weighted slice at the T11–T12 level demonstrates a well-circumscribed, hyperintense, CSF-filled myelomeningocele sac protruding dorsally through the vertebral defect (blue arrow). Within this fluid-filled pouch is a heterogeneous soft-tissue mass measuring approximately 156 × 154 mm, with intermediate T2 signal and patchy areas of low signal intensity corresponding to fibrosis or necrosis. The lesion indented the adjacent paraspinal musculature and showed focal nodular thickening along its wall, suggestive of exophytic tumor growth. BB (right): A midsagittal T2-weighted image reveals the myelomeningocele sac extending from T11 to S1, housing the irregular intraluminal mass that displaces and infiltrates the dorsal spinal cord. The tumor appears heterogeneously hyperintense, with central regions of hypointensity consistent with necrosis or keratin debris. Above the sac, the cerebellar tonsils herniate through the foramen magnum, confirming Arnold–Chiari II malformation (blue arrow). A ventriculoperitoneal shunt catheter was also visible, coursing from the cranial vault toward the abdomen

The tumor was staged according to the TNM classification and AJCC criteria as Stage IIIA (T3N0M0). This classification was based on a tumor size of 15–16 cm, invasion beyond the subcutaneous fat with dural contact, and a high-risk paravertebral location.

Following a comprehensive preoperative evaluation, a multidisciplinary surgical team consisting of a surgical oncologist, neurosurgeon, and plastic surgeon proceeded with the operation. An elliptical skin incision was made extending down to the lumbar aponeurosis, allowing en bloc resection of the tumor mass. Notably, no clear plane of dissection was identified between the tumor and myelomeningocele, reflecting tumor invasion into the spinal cord.

During the operation, the tumor was carefully dissected along the posterior wall of the vertebral body and completely excised. To ensure full removal, durotomies were performed at the cranial and caudal limits of the spinal cord (Fig. 3). The surgical specimen measured approximately 15–16 cm at its greatest dimension, consistent with intraoperative observations.

Fig. 3.

A Close-up intraoperative view showing the depth and complexity of surgical resection. Exposed neural elements and spinal cord tissue are visible in the central portion (Blue Arrow), with durotomy sites evident where the cranial and caudal margins were addressed. B Intraoperative photograph showing the surgical defect immediately after en bloc tumor resection. The circular wound bed reveals the exposed posterior vertebral elements and spinal canal contents at the base (black arrow). The defects measure approximately 15–16 cm in diameter. C The specimen demonstrates the characteristic cauliflower-like, exophytic morphology typical of squamous cell carcinoma, with areas of central necrosis, ulceration, and viable tumor tissue

Pathological examination revealed that the deep margin corresponded to the posterior dural surface of the spinal cord. The tumor extended up to the dura mater but did not penetrate it. Inspection through the durotomies showed inflammatory changes along the inner dural layer, yet no evidence of tumor invasion into the cerebrospinal fluid or spinal cord parenchyma. The peripheral margins included wide, uninvolved segments of skin and subcutaneous tissue, measuring at least 1–2 cm circumferentially around the tumor.

The large 15–16 cm posterior defect necessitated a multilayered reconstruction. Deep muscular support was achieved through latissimus dorsi advancement, providing well-vascularized bulk and protection for neural and soft tissues. Bilateral V-Y advancement flaps were used to achieve primary cutaneous closure without tension while preserving sensory integrity. This reconstructive strategy was favored over skin grafting—deemed inadequate due to limited vascularization and direct spinal cord exposure—and over single-flap techniques, which lacked sufficient tissue volume for both defect coverage and dural protection (Fig. 4).

Fig. 4.

Patient’s back immediately after reconstruction of the large posterior defect. Bilateral V-Y advancement flaps were transposed centrally, meeting along a T-shaped suturing line. Three surgical drains exited the superior flap edges. Latissimus dorsi muscle advancement underlies the flaps, providing a robust bulk

Reconstruction resulted in robust, durable soft-tissue coverage. Concurrent debridement of existing pressure ulcers was performed to optimize wound healing and reduce postoperative complications.

Final histopathology confirmed a diagnosis of well-differentiated SCC with the following features: nests and sheets of keratinizing epithelial cells exhibiting moderate nuclear pleomorphism, focal perineural invasion PNI involving two small-caliber nerves, a mitotic rate of 8–10 per high-power field, and areas of central necrosis and ulceration consistent with Marjolin-type degeneration (Fig. 5).

Fig. 5.

histological features (A) Hematoxylin & Eosin-stained section at low magnification x2 showing infiltration of dermis and hypodermis by an epithelial malignant proliferation arranged in clusters. B At high magnification x40 tumor cells had atypical nuclei with variable degrees of pleomorphism and abundant eosinophilic cytoplasm. There were numerous dyskeratotic cells (red arrows)

No dural invasion was identified histologically; intraoperative findings of dural adherence represented contact only, without evidence of cerebrospinal fluid penetration. All surgical margins were free of tumor, confirming complete excision with no microscopic residual disease. The absence of malignant cells at the inked margins in all planes further supported the curative nature of the resection. Owing to the tumor’s close dural relationship, an aggressive margin strategy was employed, and adjuvant radiotherapy was subsequently recommended.

The patient tolerated the operation well and experienced an uneventful postoperative recovery.

The decision to administer adjuvant locoregional radiotherapy was driven by several high-risk features identified in the final pathology and clinical assessment, in alignment with current NCCN and published recommendations. These included tumor invasion beyond the subcutaneous fat with dural contact and inflammatory changes—corresponding to an AJCC T3 classification—a large size measuring 15–16 cm in maximum diameter, and a paravertebral/spinal location, which is inherently associated with increased recurrence risk due to the challenge of securing wide resection margins near critical neural structures. The patient achieved complete margin clearance with 1–2 cm peripheral margins and a clear deep margin at the dural surface, confirming R0 resection. The patient subsequently underwent locoregional radiotherapy with a dose of 50 Gy.

At three months postoperatively, the patient’s neurological status improved from ASIA Grade B to C, with partial recovery of motor and sensory function and a lower extremity motor score increase from 0 to 8. By 12 months, he reached ASIA C–D, achieving independent wheelchair mobility with arm-drive assistance. At 24 months, neurological function remained stable at Grade C–D, without further decline (Table 2).

Table 2.

Neurological and functional outcomes

Timeline	ASIA Grading	Lower Extremity Motor Score	Neurological Status	Functional Outcomes	Other Clinical Notes
Baseline (Preoperative)	ASIA Grade B	0 (absent motor function)	Flaccid paraparesis; preserved perianal sensation and anal tone; upper extremity strength 5/5 intact	Dependent for ADLs; urinary incontinence; pressure ulcers on buttocks; limited mobility	Spinal cord infiltrated by tumor from T11–S1; chronic spinal cord compression from Arnold–Chiari II and MMC mass
3 Months Postoperatively	ASIA Grade C	8 (partial recovery of motor function)	Improved from Grade B; partial recovery of motor and sensory function	Progressive functional gains beginning	En bloc tumor resection completed; radiotherapy initiated
12 Months Postoperatively	ASIA Grade C–D	—	Continued neurological improvement	Independent wheelchair mobility with arm-drive assistance; seated activities and transfers using adaptive equipment	Bowel/bladder continence impaired but managed with intermittent catheterization and bowel regimen
24 Months Postoperatively	Grade C–D (stable)	—	Stable neurological function; no further decline	Maintained independence in wheelchair mobility; independence in seated ADLs; pressure ulcers completely healed	Disease-free status; no local recurrence; no new neurological deficits

Key Improvements Over 24 Months:

• ASIA Grade progression: B → C → C–D (sustained improvement)

• Motor score: 0 → 8 within first 3 months, with continued functional gains

• Functional independence: Progressed from dependent to independent in wheelchair mobility and basic ADLs

• Wound healing: Pressure ulcers resolved completely following surgical reconstruction

• Oncological status: 2-year disease-free survival with no evidence of recurrence

The patient demonstrated significant neurological and functional recovery despite complex spinal cord involvement, attributed to younger age (19 years), preserved baseline sensory function (favorable ASIA Grade B with perianal sensation intact), complete tumor resection (R0), and adjuvant radiotherapy in a multidisciplinary care setting

Functionally, the patient regained independence in seated activities and transfers using adaptive equipment. Bowel and bladder continence remained impaired but was effectively managed through intermittent catheterization and a bowel regimen, representing marked improvement from his preoperative dependence. Pressure ulcers healed completely following flap coverage and conservative care, and no new neurological deficits were observed.

At two years of post-treatment, he remains clinically disease-free, with no evidence of local recurrence.

Literature review methodology

Search strategy

PubMed and Google Scholar (1967–2025) using keywords: “myelomeningocele AND squamous cell carcinoma,” “neglected myelomeningocele,” “Marjolin’s ulcer spine”.

Inclusion criteria

• Case reports with histologically confirmed SCC in MMC

• English-language publications

Exclusion criteria

• SCC in spina bifida occulta or other spinal conditions without meningocele

• Non-English publications

Data Extraction: Age, sex, tumor location, CSF fistula status, surgical approach, resection completeness (R0/R1/R2), histologic grade, adjuvant therapy, follow-up duration, outcome.

Study quality note

Case-report heterogeneity limits formal meta-analysis; margin documentation and long-term follow-up incomplete in pre-1990s literature.

Discussion

MMC, a neural tube defect occurring in 0.5-2 per 1000 live births, requires early postnatal surgical closure to prevent infection and preserve neurological function [1]. Malignant transformation, specifically SCC, is an exceptionally rare but severe complication of chronic, untreated MMC, and represents only the 16th documented case in the literature [2–16].

This malignancy likely arises through mechanisms analogous to Marjolin’s ulcer, wherein chronic irritation, ulceration, infection, and impaired local immune surveillance at unprotected MMC sites create a microenvironment favoring neoplastic transformation [9, 19]. In this patient, the long-standing ulcerated MMC with persistent cerebrospinal fluid leakage and polymicrobial colonization likely amplified these processes and accelerated malignant transformation within the chronically damaged lumbar defect [22, 23].

Patients with untreated MMC typically present with the classic triad of neural tube defects, Arnold-Chiari type II malformations (characterized by cerebellar tonsillar herniation [17, 18]), and hydrocephalus. Associated neurological deficits (e.g., paraparesis and incontinence) and pressure ulcers further complicate management [1, 19]. Diagnosing SCC within these chronic wounds is challenging because of altered tissue and frequent infections, but rapid enlargement, ulceration, foul odor, and a cauliflower-like appearance should raise suspicion [9].

The 15 previously published cases (1975–2025) demonstrate predominantly male predominance (73%, 11/15), median age 29 years, and strong anatomic predilection for lumbar/lumbosacral sites (80%, 12/15)—regions with highest MMC prevalence. Notably, 67% (10/15) of prior cases documented cerebrospinal fluid fistula, a feature strongly associated with accelerated malignant transformation [2–16].

Comprehensive historical analysis reveals aggregate mortality of 53% (8/15 deceased), with mean follow-up < 2 years among survivors [2–16]. Strikingly, only 20% of prior cases (3/15) achieved complete oncologic resection (R0) with clear margins [2–16]. In contrast, the current case achieved R0 resection with 1–2 cm peripheral margins and clear deep margin at the dural surface, confirmed on pathology. Contemporary evidence demonstrates that positive or close margins in cutaneous SCC are associated with 33.8% metastasis and 14.7% recurrence rates, compared to < 6% recurrence with negative margins [24, 25]. This margin achievement despite dural involvement represents a critical contributor to superior prognosis.

Only 27% of prior cases (4/15) received adjuvant radiotherapy, reflecting historical uncertainty regarding benefit [2–16]. However, modern evidence demonstrates substantial benefit: a landmark study comparing surgery alone versus surgery with adjuvant radiotherapy in high-risk cutaneous SCC with perineural invasion showed 5-year disease-free survival of 100% (with RT) versus 68.8% (without RT, p = 0.01)—a 31.2% absolute improvement with zero local recurrence and zero nodal metastases in the RT-treated group, compared to 11% nodal metastasis rate without RT [26].

The current case exhibited documented small-caliber perineural invasion (PNI) in 2 nerves, a high-risk feature representing an independent predictor of recurrence. PNI increases nodal metastasis risk 4-fold to 14-fold depending on additional risk factors, and modern NCCN guidelines recommend adjuvant radiotherapy for SCC with PNI in the context of high-risk features such as dural contact and large tumor size (15–16 cm) [27]. The current case’s receipt of adjuvant radiotherapy aligns with contemporary evidence-based standards and substantially contributed to the exceptional disease-free outcome [28].

Analysis of prior cases reveals younger age and favorable baseline neurological status as favorable prognostic indicators [2–16]. The 5 surviving cases predominated in younger patients (ages 11–29 years), whereas deceased cases included older patients with advanced comorbidity [6, 13]. The current case, at age 19 with ASIA Grade B paraplegia (preserved perianal sensation and anal tone), possessed favorable prognostic indicators predictive of neuroplasticity. Post-operative progression from ASIA Grade B to Grade C–D over 24 months, achieving independent wheelchair mobility and activities of daily living independence, demonstrates that young age and preserved baseline sensory function facilitate functional recovery.

A critical observation from mortality analysis is that 37.5% of deaths (3/8 deceased patients) resulted from infectious complications [3, 4, 12], reflecting MMC patients’ vulnerability to infection given breached anatomic barriers and malignancy-associated immunosuppression. The current case’s rapid diagnosis and immediate multidisciplinary surgical intervention (within 2 weeks of presentation) contrasts sharply with delayed presentations in prior series (median latency 28 years from chronic wound to diagnosis in Marjolin’s ulcer literature) and likely mitigated infection risk while permitting complete tumor resection before metastatic dissemination.

This case exemplifies modern multidisciplinary management integrating surgical oncology for en bloc tumor resection, neurosurgery for durotomy and spinal cord assessment, and plastic surgery for complex soft-tissue reconstruction—now regarded as standard care for complex spinal malignancies [20, 29–34]. In contrast, many earlier reports from the 1970–1980 s describe predominantly single-specialty management with inferior outcomes [2–16]. Optimal treatment relies on coordinated multidisciplinary planning with en bloc resection and wide margins, followed by tailored reconstructive strategies such as bilateral V–Y advancement combined with latissimus dorsi flaps for durable coverage of large posterior defects.

This case highlights the need for early operative treatment to prevent this devastating complication, especially in resource-poor settings, where treatment delays occur [9]. It also underlines the need for vigilant surveillance in untreated patients for signs of malignant transformation [19]. The good outcome in this case (disease-free at 2 years) is in stark contrast to the poor prognosis described in previous cases [7–9, 12, 15, 16].

Conclusion

This is a rare but preventable complication of untreated myelomeningocele, which demonstrates the importance of early intervention in neural tube defects. Successful treatment requires multidisciplinary care, surgical resection, and adjuvant therapies. While this patient did well, this case highlights the importance of access to health care and early treatment of congenital anomalies to prevent such complications. Ongoing research and access to health care are necessary to reduce the occurrence of malignant transformation into untreated tube defects.

Abbreviations

SCC

Squamous cell carcinoma

MMC

myelomeningocele

Author contributions

Concepts: NBA, design, and definition of intellectual content: OJ, Literature search: MB, Clinical studies: NBA and OJ, Data acquisition: NBA and OJ, Materials: NBA, OJ and AK, Data analysis: MB, Statistical analysis: -; manuscript preparation and editing: MB, Manuscript review: TBD, Guarantor/Supervision: TBD.All the authors have reviewed the manuscript.

Funding

This study did not receive any specific grants from funding agencies in the public, commercial, or not-for-profit sectors.

Data availability

All data generated or analysed during this study are included in this published article and its supplementary information files.

Declarations

Ethics approval and consent to participate

Ethical approval was waived by the Salah Azaiez Institute Ethics Committee as per institutional policy regarding case reports. Written informed consent was obtained from the patient’s mother because of mental disability for the publication of this case report and any accompanying images. This study was made according to Helsinki principles.

Consent for publication

Written informed consent was obtained from the patient’s mother because of a mental disability.

Competing interests

The authors declare no competing interests.