Management of bone cement leakage after percutaneous vertebroplasty in a geriatric patient with multimorbidity: a case report

1 Introduction

Osteoporotic vertebral compression fracture (OVCF) is a common complication of osteoporosis and can lead to vertebral collapse, chronic refractory pain, and increased mortality. PVP is widely used for OVCF because of rapid pain relief, minimal invasiveness, and short recovery (1). However, bone cement leakage remains one of the most frequent adverse events of PVP (2). The reported incidence of cement leakage after PVP can be as high as 54.7% (3). Although most leaks are asymptomatic, intraspinal leakage may cause neurological deficit through mechanical compression, thermal injury during polymerization, or secondary ischemia.Severe osteoporosis with markedly reduced bone mineral density is a recognized risk factor for leakage (4–7). In elderly patients with multiple comorbidities, both the risk of leakage-related complications and the complexity of subsequent management increase substantially. Herein, we report a case of symptomatic intraspinal bone cement leakage after PVP in a patient with severe osteoporosis and multiple comorbidities, and describe the diagnostic and therapeutic process in detail, in order to provide a practical reference for similar complex scenarios.

2 Case report

2.1 Current medical history

An 84-year-old female patient was admitted to the pain department of our hospital with a seven-day history of progressively worsening low back pain accompanied by abdominal pain. One month prior to admission, she had undergone PVP at the T10 level for a thoracic vertebral compression fracture. Postoperatively, she developed persistent low back pain and abdominal pain. Because she had a history of herpes zoster, the patient initially attributed her symptoms to postherpetic neuralgia and therefore sought treatment in the pain department. However, her low back pain and abdominal pain continued to worsen despite conservative management. She subsequently developed bilateral lower limb numbness and weakness that did not improve, along with difficulty urinating and constipation. Due to the lack of symptom relief and the emergence of progressive neurological deficits, she was transferred to the Department of Spine Surgery for further evaluation and management.

The patient’s clinical course and key events are summarized in Table 1.

Table 1. Clinical timeline of the case.

On physical examination, the patient was in obvious distress. Pulmonary auscultation revealed crackles and bronchial breath sounds. There was thoracic kyphosis with limited spinal flexion and extension. Marked tenderness and percussion pain were noted at the thoracolumbar junction. Bilateral lower extremities showed pitting edema. Muscle strength was graded as Medical Research Council (MRC) grade 2 in the iliopsoas, quadriceps femoris, tibialis anterior, extensor hallucis longus, and triceps surae bilaterally. Hypoesthesia was present over the skin of both lower limbs. Knee and ankle jerks were brisk (+++), while Babinski signs were negative bilaterally. Perineal hypoesthesia, weakened anal reflex, and poor anal sphincter contractility were also observed, along with scattered ecchymoses in the lumbosacral region and posterior thighs. Bladder ultrasound demonstrated an overdistended bladder with no urinary sensation even upon compression, consistent with impaired urinary sensation secondary to spinal cord compression.

Anteroposterior radiographs of the thoracic spine showed high-density bone cement filling within the T10 vertebral body following previous vertebroplasty (Figure 1A). Sagittal CT reconstruction revealed bone cement leakage into the spinal canal at the T10 level, with associated thoracic spinal stenosis and spinal cord compression (Figure 1B). Axial thoracic CT demonstrated bone cement leakage into the spinal canal from the left posterior aspect of the T10 vertebral body, with compression of the dural sac and nerve roots (Figure 1C); Electrocardiography revealed atrial premature beats and complete right bundle branch block. Lower extremity vascular ultrasound showed postoperative changes of deep vein thrombosis in both calves, with the IVC filter in normal position.

2.2 Past medical history

The patient had a long-standing history of grade 3 hypertension (high cardiovascular risk) and had been receiving regular long-term pharmacotherapy to maintain stable blood pressure. She also had a multi-year history of coronary artery disease, complicated by premature atrial contractions, atrial tachycardia, and complete right bundle branch block. She had previously been diagnosed with deep vein thrombosis of the bilateral calves and had undergone IVC filter implantation. Additional comorbidities included old rib fractures, hiatal hernia, scoliosis, thoracic spinal stenosis, and neurogenic bladder.

2.3 Treatment course

Immediately after admission, a MDT consultation for this complex case was promptly convened, with specialists from the following departments participating: Department of Cardiology, Department of Respiratory and Critical Care Medicine, Department of Neurology, Department of Anesthesiology, Department of Endocrinology, Genetic and Metabolic Diseases, Department of Nephrology, Department of Hematology, Department of Vascular Surgery, and Department of Clinical Nutrition. The MDT confirmed the definitive diagnoses of space-occupying lesion in the thoracic spinal canal, thoracic spinal cord injury with incomplete paraplegia of both lower extremities, and thoracic osteoporotic pathological fracture (T10). The patient presented with progressively aggravated lumbodorsal pain, numbness and weakness of both lower extremities, which showed no response to prior conservative treatment and severely impaired her activities of daily living; thus, a clear surgical indication was identified.

Postoperative neurological deterioration in this elderly patient with multiple comorbidities required careful differential diagnosis. Potential causes included acute ischemic stroke (given her history of old cerebral infarction), progression of pre-existing lumbar spinal stenosis or cauda equina syndrome. Brain MRI showed no new ischemic lesions, and there was no significant progression of lumbar stenosis. After multidisciplinary consultation, it was ultimately determined that the bilateral lower limb weakness and sensory disturbances were caused by intraspinal bone cement leakage with spinal cord compression at the T10 level, which was confirmed by thoracic CT and intraoperative findings during revision surgery.For the subsequent treatment strategy, the MDT noted that the patient was of advanced age, with an extremely high perioperative risk of major adverse events including heart failure, acute myocardial infarction, respiratory failure, stroke, and renal failure; therefore, postoperative transfer to the intensive care unit for continuous monitoring and supportive care was recommended. In view of the patient's concurrent pleural effusion, chronic pulmonary inflammation, pulmonary edema, osteoporosis, nutritional risk, acute kidney injury, and intermuscular venous thrombosis, the MDT put forward the following standardized recommendations: (1) IVC filter implantation was suggested to reduce the incidence of pulmonary embolism; (2) Daily supplementation of 800–1200 mg elemental calcium and 1000 IU vitamin D3 was prescribed, with regular re-examination of renal function; (3) Anti-infective therapy, moderate diuresis, and a high-protein diet were recommended; (4) Low-dose anticoagulant therapy should be initiated; (5) Supplementary examinations including BMD test, serum calcium, parathyroid hormone, and urinary system ultrasound should be completed when clinically appropriate, with further workups including immunofixation electrophoresis, serum free light chain assay, reticulocyte count, serum protein electrophoresis, anemia panel, antinuclear antibody test, and bone marrow aspiration with biopsy if necessary.

Following the MDT consultation, the patient was initially managed with comprehensive conservative and symptomatic treatment. For her pre-existing Grade 3 hypertension, coronary artery disease, and arrhythmias, rosuvastatin, Wenxin Granule, and nifedipine sustained-release tablets were administered for blood pressure control and cardiac rhythm management. For abdominal distension and difficult defecation, symptomatic treatment with New Compound Aloe Capsules was given. Coronary computed tomography angiography and pulmonary computed tomography angiography were subsequently performed, which confirmed the diagnosis of pulmonary embolism. Anticoagulant therapy was clinically indicated for this condition; however, given the presence of subcutaneous ecchymosis and the small lesion area of PE, temporary low-dose anticoagulation was prioritized. Following the specialist recommendation from the Department of Respiratory Medicine, enoxaparin 0.2 mL was administered via subcutaneous injection every 12 hours (q12 h). After the patient's clinical condition improved, enoxaparin was discontinued and switched to oral rivaroxaban 10 mg once daily (qd) for long-term anticoagulation, in accordance with the consultation advice from the Department of Vascular Surgery.

As the patient was unable to cooperate with pulmonary function testing due to difficulty standing and labored breathing, she was instructed to perform balloon-blowing exercises at bed rest to improve pulmonary function. Additional symptomatic medications were prescribed, including Xianling Gubao Capsule, mecobalamin tablets, esomeprazole magnesium enteric-coated tablets, calcium carbonate and vitamin D3 chewable tablets, and calcitriol soft capsules. Quantitative computed tomography examination showed that the patient's average vertebral BMD was 37.6 mg/cc, which was far below the diagnostic reference threshold of 80 mg/cc, confirming severe osteoporosis. After her clinical condition was stabilized, teriparatide 20 μg was administered via subcutaneous injection once daily for anti-osteoporosis treatment. Relevant follow-up examinations were scheduled to re-evaluate the perioperative surgical risk, and elective surgery was planned after optimization of the patient's physical condition and functional status.

We conducted regular follow-up evaluations of the patient's neurological and functional status at multiple time points using the Visual Analogue Scale (VAS) for pain, ASIA Impairment Scale, Barthel Index for activities of daily living, and Medical Research Council (MRC) muscle strength grading. Preoperatively, the patient presented with severe low back pain (VAS 7), incomplete paraplegia (ASIA C), bilateral lower limb weakness (MRC 2/5), sensory hypoesthesia of bilateral lower extremities and perineal area, and impaired urinary function. Following revision surgery, progressive and significant improvement was observed, Unfortunately, we were unable to obtain imaging data at 1 month and 6 months postoperatively. Detailed assessments are summarized in Table 2.

Table 2. Neurological and functional assessments at different time points.

2.4 Surgical procedure

The patient underwent revision surgery consisting of thoracic laminectomy and decompression, pedicle screw fixation with bone cement augmentation, and intertransverse bone grafting. Under general anesthesia, the patient was placed in the prone position. After routine skin preparation and sterile draping, C-arm fluoroscopy was used to localize the T10 level and confirm the extent of previous bone cement leakage and spinal stenosis. A posterior midline incision was made centered on the T10 spinous process. The paravertebral muscles were dissected to expose the lamina from T8 to T12. Partial laminectomy was performed at the T10 level, and leaked bone cement fragments within the spinal canal were thoroughly removed to achieve adequate decompression of the spinal cord (Figures 2A–C).Two pedicle screws were inserted at each of the T8, T9, T11, and T12 levels under fluoroscopic guidance. Connecting rods were placed and secured after confirmation of satisfactory alignment and screw position. Bone cement augmentation was performed at the T8, T9, T11, and T12 levels to enhance screw purchase in the osteoporotic bone. An appropriate amount of autologous bone mixed with artificial bone was placed over the decorticated lamina. After meticulous hemostasis, two drainage tubes were placed, and the incision was closed layer by layer. Intraoperative blood loss was approximately 200 mL. The patient's vital signs remained stable, and no iatrogenic neurological injury occurred.

2.5 Postoperative management

After the operation, the patient was returned to the ward with continuous electrocardiographic monitoring and oxygen inhalation, and her vital signs were continuously monitored until stabilization. The following pharmacotherapy was administered: cefuroxime for surgical site infection prophylaxis, naproxen sodium for analgesia, enoxaparin for anticoagulation, subcutaneous teriparatide injection for anti-osteoporosis treatment, sodium aescinate for relieving tissue edema, and pantoprazole for gastric mucosa protection. Low-frequency pulse electrical therapy was performed to promote the recovery of gastrointestinal function. The incision drainage tube was kept unobstructed, and was removed 24–48 hours postoperatively according to the drainage volume; regular dressing changes were performed to monitor the healing of the surgical incision.

The analgesic regimen was adjusted according to the Visual Analogue Scale pain score, with a gradual transition to oral analgesic preparations. The patient was given early guidance on turning in bed and limb movement to prevent pressure injuries and deep vein thrombosis. Nifedipine was continued to maintain stable blood pressure, with dynamic monitoring and timely dose adjustment of relevant medications. Regular re-examination of lower extremity vascular ultrasound was performed. Postoperative thoracic CT/MRI was conducted to evaluate the position of bone cement, vertebral stability, and the effect of spinal canal decompression. Routine monitoring of complete blood count, liver and kidney function, coagulation function, and BMD was performed regularly, and the treatment regimen was adjusted according to the examination results. Long-term follow-up was arranged to monitor the control of underlying comorbidities and the recovery of spinal function.

Postoperatively, the patient experienced significant relief from thoracodorsal pain and lower extremity numbness and weakness, with no new neurological deficits observed. Sagittal CT reconstruction at one week post-surgery demonstrates well-positioned pedicle screw instrumentation, restored physiological spinal alignment, uniform bone cement distribution in the affected vertebral body, complete removal of intraspinal leaked cement, and adequate spinal canal decompression (Figure 3A); Sagittal CT reconstruction at three months of follow-up confirms stable placement of the internal fixation devices without loosening or breakage, uniform bone cement distribution without re-leakage, maintained spinal stability, persistent patency of the spinal canal, and no recurrence of spinal cord compression (Figure 3B).

3 Discussion

In this report, we present a case of symptomatic intraspinal bone cement leakage after percutaneous vertebroplasty (PVP) in an elderly patient with severe osteoporosis and multiple comorbidities. Although cement leakage is a common adverse event after PVP, symptomatic intraspinal leakage requiring surgical intervention remains uncommon. Hsieh et al. reported only 4 surgically treated cases among 3175 PVP procedures, and Saracen et al. identified only 1 patient requiring surgery for neurological deficit among 9 cases of intraspinal leakage (8, 9).

The key lessons from this case concern the mechanism of delayed leakage and the timing of revision surgery. Regarding the primary PVP, a unipedicular approach via the left pedicle was used at the T10 level, and approximately 5 mL of low-viscosity bone cement was injected in stages under real-time fluoroscopic monitoring by an experienced spine surgeon. We attribute the delayed symptomatic intraspinal leakage to three factors: the use of low-viscosity cement, which is more prone to extravasation; staged injection, which created a relatively weak junction between the two cement masses; and severe osteoporosis, which facilitated subsequent displacement of the cement segments at that junction into the spinal canal. These observations underscore the importance of preventive measures during primary PVP in high-risk osteoporotic patients, including preferential use of high-viscosity cement, strict control of injection volume and rate, and continuous fluoroscopic monitoring, so that open revision and its attendant risks may be avoided whenever possible (10, 11).

Open revision remains the standard treatment for symptomatic intraspinal cement leakage with progressive neurological deficit (12).Rathod et al. reported a case of intra-spinal epidural cement leakage during vertebroplasty that was successfully managed with immediate decompression, cement removal, and posterior instrumentation (13).In this patient, after thorough decompression and removal of leaked cement, pedicle screws were placed at T8, T9, T11, and T12 with cement augmentation at these levels only. No additional cement was injected into the T10 vertebral body itself, in order to enhance screw purchase in osteoporotic bone while minimizing the risk of recurrent leakage into the decompressed canal. The procedure was performed under direct visualization with careful volume control and real-time fluoroscopy; no further extravasation was observed.

A second clinical challenge was the coexistence of progressive neurological deterioration and active pulmonary embolism. Cardiopulmonary symptoms had improved by 17 October 2025, whereas bilateral lower-limb numbness and weakness continued to worsen. After comprehensive reassessment on 19 October 2025 (including CTPA, lower-extremity venous ultrasound, and laboratory evaluation), correction of electrolyte imbalance, and placement of an inferior vena cava filter, the patient's overall condition stabilized and revision surgery was undertaken on 23 October 2025. Perioperative anticoagulation was managed in an individualized manner in accordance with clinical guidelines, with temporary interruption of oral anticoagulation and enoxaparin bridging; no perioperative thromboembolic or major hemorrhagic events occurred. This sequence illustrates that, when neurological deficit progresses alongside active pulmonary embolism, open revision should be timed after cardiopulmonary improvement and thromboembolic risk reduction rather than performed immediately or deferred indefinitely.

This study has several limitations. First, as a single case report, the findings cannot be generalized and causal inference is limited. Second, there is no comparison group, which restricts contextualization of the results. Third, MRI after the onset of symptomatic leakage was not available, which limits detailed assessment of cord signal change, some specific technical details regarding the primary PVP procedure were not available. Fourth, the follow-up period of six months remains relatively short for fully evaluating long-term outcomes such as construct stability, neurological recovery, and quality of life in a geriatric patient. Fifth, complete imaging data at all follow-up time points (particularly at one month and six months) were not available. Finally, the case originates from a single institution in China, which may limit the generalizability of the findings to other healthcare settings.

Finally, this case provides critical clinical implications for the management of PVP-related bone cement leakage. Necessary preventive measures must be implemented for patients at high risk of cement leakage during PVP. A recent meta-analysis demonstrated that high-viscosity bone cement was associated with a significantly lower leakage rate compared with low-viscosity cement during percutaneous vertebroplasty (14).For elderly patients with osteoporotic fractures and multiple comorbidities, the decision-making for primary PVP should be extremely prudent, with a thorough preoperative assessment of the extremely high risk of cement leakage. Intraoperatively, strategies including the use of high-viscosity bone cement and strict control of cement injection volume should be adopted to minimize the risk of leakage. Once symptomatic cement leakage occurs, timely evaluation of neurological function and spinal stability should be performed, and open surgical intervention should be implemented decisively if clinically indicated. Meanwhile, The cornerstone of successful clinical management of such complex cases lies in the meticulous optimization of the patient's systemic condition and MDT collaboration. The implementation of multidisciplinary team meetings in complex spine surgery can significantly optimize clinical treatment decisions and help reduce the incidence of perioperative complications (15).

4 Conclusion

This case describes the management of symptomatic intraspinal cement leakage after PVP in an elderly patient with multiple comorbidities. Comprehensive preoperative assessment, careful intraoperative technique, and multidisciplinary perioperative care remain essential. We suggest that high-viscosity cement with controlled injection and continuous fluoroscopy be preferred during primary PVP in severe osteoporosis, and that open revision in the setting of progressive neurological deficit and active pulmonary embolism be timed after cardiopulmonary improvement and reassessment of the embolism.

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Footnotes

Edited by: Siying Song, UT MD Anderson Cancer Center, United States

Reviewed by: Yu Qiao, Technical University of Munich, Germany

Nino Arturo Ccallalli-Ruíz, Antenor Orrego Private University, Peru

AbbreviationsOVCF, steoporotic vertebral compression fracture, PVP, percutaneous vertebroplasty, MDT, multidisciplinary team, IVC, inferior vena cava, BMD, bone mineral density.