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22 May 2026: Articles  Mexico

Delayed Diagnosis of Bilateral Posterior Shoulder Fracture–Dislocation Following a Seizure: A Case Report

Challenging differential diagnosis, Unusual or unexpected effect of treatment, Rare coexistence of disease or pathology

César Alejandro Jiménez-Aroche ABCDEFG 1*, Juan Ramón Jiménez Castro BDEFG 1, José Luis Millet Herrera ABDEF 1, Laurence José Conway Restrepo BCEFG 1, David Gerardo Garza Cruz ABCDF 1, José Eduardo Miranda Mayén BCDFG 1, Javiera Irribaren Bravo BCDF 1, Roberto Irribaren Gómez ABCDEFG 1

DOI: 10.12659/AJCR.952420

Am J Case Rep 2026; 27:e952420

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Abstract

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BACKGROUND: Bilateral posterior shoulder fracture–dislocation can be caused by forced internal rotation during a seizure and requires management with combined open reduction procedures to address instability and fractures to restore function. This report describes the case of a 27-year-old man with a delayed diagnosis of bilateral posterior shoulder fracture–dislocation following a seizure managed by bilateral open reduction, fixation of the greater tuberosity, biceps tenodesis, and subscapularis anchor repair using a deltopectoral approach.

CASE REPORT: A 27-year-old man with no prior history of epilepsy presented with bilateral shoulder pain and severe functional limitation following a tonic–clonic seizure. Initial evaluation did not include shoulder imaging, resulting in delayed diagnosis. Over the following weeks, he developed progressive pain, weakness, and restriction of motion. Radiographs and computed tomography (CT) confirmed bilateral posterior shoulder fracture–dislocation with associated greater tuberosity fractures. Magnetic resonance imaging (MRI) demonstrated preserved rotator cuff integrity. He underwent bilateral open reduction through a deltopectoral approach, including fixation of the greater tuberosity, biceps tenodesis, and subscapularis repair with suture anchors. Both shoulders were immobilized for 3 weeks, followed by structured physiotherapy. At final follow-up, the patient had achieved full, pain-free range of motion (ROM), with significant functional improvement reflected by an increase in Constant (a validated clinical scoring system for shoulder function) scores from 4 points to 95 points bilaterally.

CONCLUSIONS: Early recognition of posterior shoulder dislocation is essential to avoid chronic disability. However, even in delayed cases, anatomical reconstruction combined with soft tissue repair and structured rehabilitation can restore excellent shoulder function when joint integrity is preserved.

Keywords: Fractures, Bone, Joint Dislocations, Orthopedics, Shoulder Dislocation, Surgical Procedures, Operative

Introduction

Posterior shoulder dislocation is the rarest form of dislocation, accounting for only 2% to 5% of cases, estimated at 1.1 per 100 000 inhabitants per year [1,2]. It is less common than anterior dislocations and contributes to the frequently troublesome diagnosis of posterior injuries. It most commonly occurs in people aged 20 to 40 years and is often attributed to high-energy trauma or preexisting neurologic disorders that predispose to explosive contractions of the muscles [2,3]. The typical mechanism involves forced adduction, internal rotation, and flexion, resulting in posterior displacement of the humeral head [4,5]. There have been relatively few posterior dislocation cases reported, but its diagnosis is important because subtle, and in most cases nonspecific, presentation can cause delayed or missed diagnosis.

This injury is missed at initial evaluation in 50% to 80% of cases, due to suboptimal anteroposterior radiographs, often leaving out axillary or scapular-Y views that are crucial for correct diagnosis [5,6]. Bilateral posterior shoulder dislocation is even rarer, accounting for less than 1% of all posterior dislocations [6], with fewer than 40 cases reported up to the early 2000s. It is usually associated with violent, synchronous contractions of muscles, particularly due to tonic–clonic seizures and electrical injuries. These forces propel the humeral head posteriorly with high energy, which frequently causes fractures or impression abnormalities [1,7,8].

Because brain injuries from seizures typically cause an acutely impaired mental status or are missed during neurologic workup, orthopedic evaluation can be delayed, with increased risk of long-term disability. When a posterior dislocation is not identified early it can progress to a chronic disorder is characterized as an unreduced position that is present for more than 3 weeks [5]. Chronic posterior dislocations are associated with thick intra-articular fibrosis, capsular contracture, and osseous dysfunction, specifically the reverse Hill-Sachs lesion, due to repetitive posterior contractions of the humeral head against the glenoid rim [5,8]. Closed restriction is increasingly impossible or hard to accomplish as these pathological changes progress and functional dysfunction worsens.

Patients generally have chronic pain, severe joint stiffness, reduced ROM, and severely limited ability to perform activities of daily living. Recent systematic reviews show that chronic posterior dislocations continue to be challenging to diagnose and treat. Basal et al [8] and Paparoidamis et al [9] stated that the size and nature of the humeral head defect must be considered in determining the most suitable surgical strategy. Moreover, Rinaldi et al [10] emphasized that misdiagnosis continues to be problematic, even in modern medical practice, showing the importance of routine use of axillary radiographs and advanced imaging when there is clinical suspicion. Management depends on the chronicity of the dislocation, the size of the humeral head defect, and soft tissue integrity. Acute dislocations can be managed with closed reduction, whereas locked or chronic cases typically require surgical intervention [6,8,10]. The recognition of bilateral presentations in the setting of seizures has increased over the last decade, with recent reports of the high burden of early misdiagnosis and the complexity of postoperative management.

Schumacher et al [11] reported bilateral posterior fracture–dislocations by hyponatremia-mediated seizure, and Wu et al [12] reported 2 cases with delayed diagnosis requiring surgery. These reports illustrate the importance of vigilance among clinicians evaluating postictal patients with shoulder problems. Simultaneously, advances in surgical techniques have widened the list of therapies for chronic cases. Although open reduction and fixation is still the most common treatment, advances in arthroscopic management, such as arthroscopic variants of the McLaughlin procedure, show promise in some cases [11,12]. Shoulder arthroplasty continues to be an attractive option for cases of extensive structural destruction or humeral head collapse, although a systematic review by Crowley et al [13] found there are more complications and revisions in this population. With the unusual incidence of chronic bilateral posterior dislocations being strongly correlated to seizures in the population, each new care report contributes to information informing optimal diagnosis timing, surgical strategies, and rehabilitation protocols.

This report describes the case of a 27-year-old man with a delayed diagnosis of bilateral posterior shoulder fracture–dislocation following a seizure, managed by bilateral open reduction, fixation of the greater tuberosity, biceps tenodesis, and subscapularis anchor repair using a deltopectoral approach.

Case Report

A 27-year-old man with no prior history of epilepsy or seizure disorders presented on January 24, 2024, with marked bilateral shoulder pain and severe functional limitation of both upper extremities. The symptoms began following a tonic–clonic seizure on January 3, 2024. At that time, he was evaluated in the emergency department, but no shoulder imaging was performed.

In the days following the event, he developed persistent generalized pain, progressive weakness, and increasing functional impairment, which ultimately led to neurologic evaluation and referral for orthopedic assessment.

On physical examination, both humeral heads were posteriorly displaced, with clinically visible “empty” glenoid fossae. Active ROM was severely limited, with forward flexion of 50° on the right side and 20° on the left, along with marked restriction of rotation, abduction, and extension (Figure 1). Neurovascular examination results were normal bilaterally.

Anteroposterior and axillary radiographs confirmed bilateral posterior shoulder fracture–dislocation (Figure 2). Given the chronicity of the injury and the potential for associated soft tissue damage, MRI of both shoulders was performed, demonstrating preserved rotator cuff integrity (Figure 3). CT further confirmed posterior dislocation of both humeral heads, associated with greater tuberosity fractures, and allowed detailed characterization of the osseous defects (Figure 4).

Surgery was performed on February 2, 2024. A bilateral deltopectoral approach was used, allowing careful debridement of intra-articular fibrosis and fracture fragments of the greater tuberosity. Open reduction of both glenohumeral joints was achieved without complications. This was followed by biceps tenodesis and fixation of the greater tuberosity using a cortical screw, along with reinforcement of subscapularis stability using suture anchors to restore anterior soft tissue integrity as shown in the postoperative radiographic and CT images of both shoulders (Figures 5, 6).

Postoperatively, both shoulders were immobilized in abduction pillows for 3 weeks. An intensive physiotherapy program was subsequently initiated, focusing on progressive strengthening and restoration of ROM. At final follow-up, the patient had achieved full, pain-free ROM with complete functional recovery (Figure 7). The Constant score improved from 4 points preoperatively to 95 points bilaterally (Figure 8).

Discussion

This case report shows that even in delayed bilateral posterior shoulder fracture–dislocation, anatomical reconstruction combined with structured rehabilitation can result in excellent functional outcomes when rotator cuff integrity is preserved.

Chronic bilateral posterior shoulder dislocation is extremely rare and accounts for <1% of the total posterior dislocations and is strongly related to seizure activity and electrical injury [1,6–8]. This rarity makes bilateral cases particularly challenging to diagnose, especially in the acute setting. Clinical findings following seizure-related injuries are often subtle, nonspecific, or easily overlooked, paradoxically when the neurologic event itself is more clinically apparent, contributing to a high risk of delayed or missed diagnosis. Diagnosis is often delayed because clinical features can be subtle, and standard anteroposterior radiographs may deceptively appear normal, accounting for the consistently high rates of missed diagnosis reported [5,6]. The absence of a true axillary view or scapular-Y projection still is a leading cause of diagnostic failure, as they are fundamental in identifying the posterior location of the humeral head.

Chronic posterior dislocations, defined as unreduced dislocations lasting >3 weeks, are characterized by severe intra-articular fibrosis and capsulolabral contracture, leading to joint mechanical obstruction to reduction. The impression defect usually appears in the anteromedial portion of humeral head, known as a reverse Hill-Sachs lesion, and is often the result of repeated engagement of the posterior glenoid margin [8]. With chronicity, these defects usually grow, making them more likely to be unstable and make surgery difficult. Clinically, patients present with progressive stiffness, weakness, and limitations in elevation and rotation, with evident posterior prominence of the humeral head. These deficits markedly hinder activities of daily living involving the upper extremities, and often present as a distinct impairment and lead to profound disability, particularly in bilateral cases, in which compensatory movement of the contralateral limb is not accomplished.

Basal et al [8], Paparoidamis et al [9], and Rinaldi et al [10] emphasize that management of chronic posterior dislocation needs to be individualized. Their analyses demonstrate that the size of the reverse Hill-Sachs defect, integrity of the lesser tuberosity and subscapularis, level of chronicity and fibrosis, glenoid morphology, and the demographic and functional demands of patients play critical roles in treatment. Small or moderate defects can be treated with soft tissue interventions such as the McLaughlin procedure or some modifications thereof, while more severe defects usually require structural bone procedures or arthroplasty. These reports emphasize that the chronic nature of the injury often makes closed reduction difficult because surgery is the mains treatment used for most patients. Recent publications also recommend surgery for long-term dislocations. Saylık and Gökkuş [14] described a neglected bilateral posterior dislocation diagnosed 15 months after injury but successfully treated surgically with a modified McLaughlin procedure, demonstrating that even very long-term cases can achieve functional improvement.

Haritinian et al [15] showed promising outcomes in 12 patients who received surgical management for chronic posterior dislocation, demonstrating the benefits of open procedures for reconstructing stability in patients with soft tissue contractions and osseous defects. Taken together, the results indicate that chronicity is not a disincentive to surgery if reconstruction is possible. Previous reports have described bilateral posterior shoulder fracture–dislocation as a rare but clinically challenging entity, usually associated with seizure activity. Huizing and Monteban reported a series of cases highlighting the high rate of delayed diagnosis and the need for individualized surgical management based on defect size and chronicity. Their findings showed that surgical treatment, particularly when anatomical reconstruction is achieved, can result in favorable functional outcomes. These observations are consistent with the present case, in which delayed diagnosis did not preclude excellent recovery after anatomical reconstruction and structured rehabilitation [16].

Reports by Schumacher et al [11] and Wu et al [12] show the need for increased suspicion regarding posterior dislocation in patients with shoulder pain after a seizure. Delayed diagnosis was a recurring theme in both reports and suggested that with a neurologic diagnostic history frequently taking precedence over musculoskeletal examination, the clinicians were overlooked an underlying traumatic injury. Their findings suggest that early imaging with adequate projections, in the presence of these issues, is key to preventing chronicity. Furthermore, both reports noted that bilateral damage can be obscured by the patient’s generalized postictal condition requiring a systematic and comprehensive clinical examination. Advances in arthroscopic therapy have increased therapeutic efficacy for chronic posterior dislocations.

Crowley et al [13] reported significant complication and revision rates in this cohort, especially in younger patients, supporting that arthroplasty should be reserved for cases with irreversible pathology or where degenerative disease is more progressed. The higher incidence of instability, loosening, and dysfunction during arthroplasty in active/younger people supports a recommendation for joint preservation when possible. Our case shows that multiple predisposing factors often lead to chronicity: acute onset after a seizure, lack of initial imaging workup, progressive functional loss, and delayed orthopedic examination.

Since the lesion is bilateral, this significantly enhances functional disability, as the patient does not have a compensatory limb to help with daily living activities. Despite these difficulties, meticulous anatomical reconstruction of the greater tuberosity and subscapularis, with progressive rehabilitation, achieved full functional recovery. The patient’s Constant score improved from 4 to 95, close to and sometimes better than cases described in the recent literature [11–16]. This impressive improvement demonstrates that even in patients with a delayed diagnosis, early treatment and rehabilitation can lead to near complete functional recovery if bone integrity and the rotator cuff remain intact. The present report also highlights many common themes in the literature.

Thorough assessment of shoulders after a seizure is crucial: pain, limited ROM, and posterior fullness should all precipitate immediate imaging, including axillary views. Prognosis is influenced by the condition of a normal rotator cuff, normal subscapularis tension recovery, and the extent of reconstruction of the anterior humeral head contour. Rehabilitation is an important factor, as chronic dislocation is associated with significant muscle wasting and capsular stiffness, and treatment of patients with longstanding dislocations relies on regular supervised physiotherapy.

Conclusions

Early recognition of posterior shoulder dislocation is essential to prevent progression to long-term disability, particularly in patients presenting after a seizure. This case demonstrates that even in delayed bilateral posterior shoulder fracture–dislocation, anatomical reconstruction combined with appropriate soft tissue repair and structured rehabilitation can result in excellent functional outcomes when joint integrity is preserved.

Figures

Clinical appearance of bilateral posterior shoulder dislocation. Physical examination demonstrates abnormal posterior prominence of both shoulders with loss of the normal deltoid contour. The humeral heads are displaced posteriorly, producing a visible “empty glenoid” appearance. Active range of motion is severely limited in both shoulders.Figure 1. Clinical appearance of bilateral posterior shoulder dislocation. Physical examination demonstrates abnormal posterior prominence of both shoulders with loss of the normal deltoid contour. The humeral heads are displaced posteriorly, producing a visible “empty glenoid” appearance. Active range of motion is severely limited in both shoulders. Anteroposterior and axillary radiographs showing bilateral posterior shoulder fracture–dislocationRadiographic evaluation demonstrates posterior displacement of both humeral heads relative to the glenoid. Loss of normal glenohumeral congruency and cortical disruption are observed, consistent with associated greater tuberosity fractures.Figure 2. Anteroposterior and axillary radiographs showing bilateral posterior shoulder fracture–dislocationRadiographic evaluation demonstrates posterior displacement of both humeral heads relative to the glenoid. Loss of normal glenohumeral congruency and cortical disruption are observed, consistent with associated greater tuberosity fractures. Magnetic resonance imaging demonstrating preserved rotator cuff integrityMagnetic resonance imaging of both shoulders shows intact rotator cuff tendons without evidence of tearing or retraction, despite chronic posterior dislocation. This finding is relevant for surgical planning and prognosis.Figure 3. Magnetic resonance imaging demonstrating preserved rotator cuff integrityMagnetic resonance imaging of both shoulders shows intact rotator cuff tendons without evidence of tearing or retraction, despite chronic posterior dislocation. This finding is relevant for surgical planning and prognosis. Three-dimensional computed tomography reconstruction of bilateral posterior fracture–dislocationThree-dimensional computed tomography images demonstrate posterior displacement of both humeral heads and associated greater tuberosity fractures. The reconstruction allows detailed evaluation of osseous defects and aids preoperative planning.Figure 4. Three-dimensional computed tomography reconstruction of bilateral posterior fracture–dislocationThree-dimensional computed tomography images demonstrate posterior displacement of both humeral heads and associated greater tuberosity fractures. The reconstruction allows detailed evaluation of osseous defects and aids preoperative planning. Postoperative computed tomography confirming anatomical reductionPostoperative CT imaging shows restoration of normal glenohumeral alignment with anatomical reduction of both humeral heads. Fixation of the greater tuberosity is visualized, with stable hardware positioning.Figure 5. Postoperative computed tomography confirming anatomical reductionPostoperative CT imaging shows restoration of normal glenohumeral alignment with anatomical reduction of both humeral heads. Fixation of the greater tuberosity is visualized, with stable hardware positioning. Follow-up anteroposterior radiograph demonstrating maintained reductionRadiographic follow-up shows preserved joint congruency and stable fixation without evidence of redislocation, hardware failure, or secondary degenerative changes.Figure 6. Follow-up anteroposterior radiograph demonstrating maintained reductionRadiographic follow-up shows preserved joint congruency and stable fixation without evidence of redislocation, hardware failure, or secondary degenerative changes. Clinical outcome at final follow-up showing full range of motionClinical photographs demonstrate symmetrical, pain-free active range of motion in both shoulders, including elevation and rotation, with no residual deformity or functional limitation.Figure 7. Clinical outcome at final follow-up showing full range of motionClinical photographs demonstrate symmetrical, pain-free active range of motion in both shoulders, including elevation and rotation, with no residual deformity or functional limitation. Functional recovery assessed by Constant scoreLine graph illustrating progressive improvement in shoulder function as measured by the Constant score (a validated clinical scoring system for shoulder function). Scores improved from 4 points preoperatively to 95 points bilaterally at final follow-up.Figure 8. Functional recovery assessed by Constant scoreLine graph illustrating progressive improvement in shoulder function as measured by the Constant score (a validated clinical scoring system for shoulder function). Scores improved from 4 points preoperatively to 95 points bilaterally at final follow-up.

References

1. Robinson CM, Aderinto J, Posterior shoulder dislocations and fracture-dislocations: J Bone Joint Surg Am, 2005; 87(3); 639-50

2. Shaw JL, Bilateral posterior fracture-dislocation of the shoulder and other trauma caused by convulsive seizures: J Bone Joint Surg Am, 1971; 53(7); 1437-40

3. Cicak N, Posterior dislocation of the shoulder: J Bone Joint Surg Br, 2004; 86(3); 324-32

4. Aydin N, Enes Kayaalp M, Asansu M, Karaismailoglu B, Treatment options for locked posterior shoulder dislocations and clinical outcomes: EFORT Open Rev, 2019; 4(5); 194-200

5. Kammel KR, El Bitar Y, Leber EH, Posterior shoulder dislocations. [Updated 2022 Sep 12]: StatPearls [Internet], 2026, Treasure Island (FL), StatPearls Publishing Available from:https://www.ncbi.nlm.nih.gov/books/NBK441919/

6. Dinopoulos HT, Giannoudis PV, Smith RM, Matthews SJ, Bilateral anterior shoulder fracture-dislocation: A case report and a review of the literature: Int Orthop, 1999; 23(2); 128-30

7. Brackstone M, Patterson SD, Kertesz A, Triple “E” syndrome: Bilateral locked posterior fracture dislocation of the shoulders: Neurology, 2001; 56(10); 1403-4

8. Basal O, Dincer R, Turk CY, Erol B, Locked posterior dislocation of the shoulder: A systematic review: EFORT Open Rev, 2018; 3(1); 15-23

9. Paparoidamis G, Koukoulias N, Dimitriadis T, Papathanasiou JV, Posterior shoulder fracture-dislocation: A systematic review of the literature and current aspects of management: Chin J Traumatol, 2021; 24(1); 18-24

10. Rinaldi VG, Coliva F, Favero A, From diagnosis to decision-making: A systematic review of the management of reverse Hill-Sachs lesions after posterior shoulder dislocations: J Clin Med, 2024; 13(7); 2085

11. Schumacher KM, Moravec A, Jonas ME, Bilateral posterior shoulder fracture dislocations from seizures due to hyponatremia: A case report: JSES Rev Rep Tech, 2022; 3(1); 94-100

12. Wu J, Li L, Wang F, Bilateral posterior fracture-dislocation of the shoulders: Two rare case reports and literature review: Medicine (Baltimore), 2020; 99(36); e22088

13. Crowley M, Ghattas Y, Collins AP, Systematic review and meta-analysis of locked posterior dislocation of the shoulder treated with shoulder arthroplasty: Improved outcomes for total shoulder arthroplasty are associated with increased age: Orthop Surg, 2023; 15(7); 1730-41

14. Saylık M, Gökkuş K, Bilateral locked posterior shoulder dislocation overlooked for 15 months treated with the modified McLaughlin procedure: A case report: Jt Dis Relat Surg, 2023; 34(1); 226-33

15. Haritinian EG, Stoica IC, Popescu R, Treatment and outcomes of chronic locked posterior shoulder dislocations: A retrospective case series: BMC Musculoskelet Disord, 2023; 24(1); 82

16. Huizing JW, Monteban PE, Bilateral posterior fracture dislocation of the shoulders: review of case reports and treatment: Acta Orthop Belg, 2020; 86(2); 193-99

Figures

Figure 1. Clinical appearance of bilateral posterior shoulder dislocation. Physical examination demonstrates abnormal posterior prominence of both shoulders with loss of the normal deltoid contour. The humeral heads are displaced posteriorly, producing a visible “empty glenoid” appearance. Active range of motion is severely limited in both shoulders.Figure 2. Anteroposterior and axillary radiographs showing bilateral posterior shoulder fracture–dislocationRadiographic evaluation demonstrates posterior displacement of both humeral heads relative to the glenoid. Loss of normal glenohumeral congruency and cortical disruption are observed, consistent with associated greater tuberosity fractures.Figure 3. Magnetic resonance imaging demonstrating preserved rotator cuff integrityMagnetic resonance imaging of both shoulders shows intact rotator cuff tendons without evidence of tearing or retraction, despite chronic posterior dislocation. This finding is relevant for surgical planning and prognosis.Figure 4. Three-dimensional computed tomography reconstruction of bilateral posterior fracture–dislocationThree-dimensional computed tomography images demonstrate posterior displacement of both humeral heads and associated greater tuberosity fractures. The reconstruction allows detailed evaluation of osseous defects and aids preoperative planning.Figure 5. Postoperative computed tomography confirming anatomical reductionPostoperative CT imaging shows restoration of normal glenohumeral alignment with anatomical reduction of both humeral heads. Fixation of the greater tuberosity is visualized, with stable hardware positioning.Figure 6. Follow-up anteroposterior radiograph demonstrating maintained reductionRadiographic follow-up shows preserved joint congruency and stable fixation without evidence of redislocation, hardware failure, or secondary degenerative changes.Figure 7. Clinical outcome at final follow-up showing full range of motionClinical photographs demonstrate symmetrical, pain-free active range of motion in both shoulders, including elevation and rotation, with no residual deformity or functional limitation.Figure 8. Functional recovery assessed by Constant scoreLine graph illustrating progressive improvement in shoulder function as measured by the Constant score (a validated clinical scoring system for shoulder function). Scores improved from 4 points preoperatively to 95 points bilaterally at final follow-up.

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American Journal of Case Reports eISSN: 1941-5923
American Journal of Case Reports eISSN: 1941-5923