Bone cement embolism causing right ventricle perforation

Abstract

Background

Bone cement embolism is one of major complications of percutaneous kyphoplasty. Although rare, the intracardiac cement embolism is potentially life-threatening, with a documented incidence of 3.9%, and it is even more infrequent if symptomatic (0.3%).

Case presentation

Herein, we reported an extremely rare case of intracardiac bone cement embolism after percutaneous kyphoplasty causing right ventricle perforation. A 70-year-old woman, experiencing sudden left chest pain with radiation to the shoulder for 9 h, was transferred to our emergency department. Two hours before onset of her symptoms, she underwent percutaneous kyphoplasty at the local hospital. The computed tomography angiography revealed that an intracardiac foreign body penetrated her right ventricle. In light of her surgical history, bone cement embolism was suspected and thus, the patient was transferred to our center. Computed tomography and echocardiography confirmed the presence of intracardiac linear-shaped foreign body perforating the right ventricle. Therefore, the patient underwent open-heart surgery and the bone cement was removed successfully.

Conclusions

Symptomatic intracardiac bone cement embolism is potentially fatal, so the rapid diagnosis and prompt treatment measures based on the cement emboli characteristics and the patient’s condition are crucial.

Background

Bone cement embolism is one of major complications of percutaneous kyphoplasty (PKP), with a reported incidence up to 4.6% in PKP [1]. It mainly occurs when the cement materials, usually polymethylmethacrylate, leak from its injection site into paravertebral veins. Pulmonary cement embolism has been widely reported, which is generally asymptomatic and has no adverse clinical outcome. However, the intracardiac cement embolism is rare and life-threatening, with a documented incidence of 3.9%, and it is even more infrequent if symptomatic (0.3%) [2].

Herein, we reported an extremely rare case of intracardiac bone cement embolism after PKP causing right ventricle perforation. Therefore, the patient underwent open-heart surgery and the bone cement emboli was removed successfully.

Case presentation

A 70-year-old woman, experiencing sudden left chest pain with radiation to the shoulder for 9 h, was transferred to our emergency department. Two hours before onset of her symptoms, she underwent PKP for L2/L3 osteoporotic compression fracture at a local hospital. Emergency coronary and pulmonary artery computed tomography angiography (CTA) revealed that an intracardiac foreign body penetrated her right ventricle (Fig. 1A) and no high-density shadow was found in the pulmonary artery. Blood tests showed elevated levels of high-sensitivity troponin I (517.4ng/L) and the electrocardiogram was normal. Given her recent surgical history, bone cement embolism causing cardiac perforation was suspected. Thus, she was transferred to our center for further evaluation and treatment. At admission, she complained of intolerable chest pain, accompanied by profuse sweating, nausea and fatigue. Additionally, the physical examination was unremarkable and no signs of hypoxemia was detected. The vital signs taken reduced blood pressure but absence of tachycardia and tachypnea (blood pressure 112/59 mmHg, heart rate 78 bpm, respiratory rate 20 counts/min). The chest computed tomography (CT) scan confirmed the presence of this intracardiac linear-shaped foreign body perforating the right ventricle with a small amount of pericardial effusion (Fig. 1B). Furthermore, the transesophageal echocardiography demonstrated a highly echogenic foreign body in the right atrium and ventricle, traversing the tricuspid annulus (Fig. 1C) and leading to mild tricuspid regurgitation. No abnormalities were detected in other valves. The size of each cardiac chamber and left ventricular systolic function were normal, and blood flow in the inferior vena cava was smooth, in the direction of returning to the heart.

Fig. 1

Image findings of intracardiac bone cement embolism. (A) Coronary CTA showed the bone cement penetrated the right ventricle (yellow arrow); (B) chest computed tomography scan and (C) transesophageal echocardiography confirmed the presence of the intracardiac bone cement (yellow arrow). CTA, computed tomography angiography

Five hours after hospitalization, the patient underwent emergency open-heart surgery, which was performed through a median sternotomy with cardiopulmonary bypass in beating heart. During the procedure, we found that the sharp tip of the bone cement penetrated the right ventricle, with blood clots wrapping around the perforation site (Fig. 2A). After right atriotomy, a white, slender bone cement was observed (Fig. 2B) and carefully removed, measuring about 7.5 cm in length and 0.2 cm in diameter (Fig. 2C). Subsequently, the perforation site was sutured, and tricuspid repair was unnecessary because the bone cement had not damaged the structure of the tricuspid valve. The details of the operation were shown in the Supplementary Video 1. The postoperative echocardiography showed no residual cement fragments in the right ventricle (Fig. 2D). The patient stayed at the intensive care unit for 8 days, she had an uneventful recovery afterwards and was discharged home 24 days after the operation. Three months after the procedure, she was in good condition and visited our outpatient clinic. The chest CT showed no obvious signs of pleural effusion or pericardial effusion (Fig. 2E). What’s more, the echocardiography detected no abnormalities except trivial tricuspid regurgitation (Fig. 2F).

Fig. 2

Intraoperative, postoperative and follow-up images. (A) showed the sharp cement penetrating the right ventricle (red arrow); (B) showed the embolized bone cement in the right atrium; (C) showed the bone cement measuring about 7.5 cm in length. (D) postoperative echocardiography showed no residual cement fragments in the right ventricle; (E) chest CT showed no obvious signs of pleural effusion or pericardial effusion, and (F) echocardiography detected no abnormalities except trivial tricuspid regurgitation (yellow arrow). CT, computed tomography

Discussion and conclusions

Pulmonary cement embolism is a well-documented complication of PKP, with an incidence up to 26% [3]. It is commonly asymptomatic and rarely results in adverse clinical outcomes [2]. In contrast, symptomatic intracardiac bone cement embolism is exceedingly rare but potentially fatal [3,4,5,6,7]. Here, we reported a case of embolized bone cement perforating the right ventricle, which was surgically extracted successfully.

Intracardiac bone cement embolism typically arises when the cement materials leaks into the paravertebral veins during PKP, travels through vena cava and lodges in the right heart, potentially leading to ventricular penetration and pericardial tamponade. Hassani et al. [2]. identified that treating multiple vertebrae in a single PKP procedure was an independent risk factor for bone cement embolism, likely due to higher cement volumes, increased technical complexity, and longer procedural times. However, the utilization of flat-panel technology seemed to decrease the risk of intracardiac cement embolism, emphasizing the critical importance of high-quality fluoroscopic guidance in preventing cement leakage [2]. In addition to rigorous intraoperative monitoring, a comprehensive preoperative evaluation of vertebral body damage, careful control of bone cement solidification during the procedure, and precise management of both injection speed and cement volume are essential to preventing bone cement leakage [8] and minimizing the risk of intracardiac or pulmonary cement embolism.

The diagnosis of intracardiac bone cement embolism is often straightforward, especially when there is a recent history of PKP. Common symptoms include chest pain radiating to the shoulder or back, chest tightness, and dyspnea. Of note, symptoms do not always appear immediately after PKP, but can also manifest months or even years after the procedure [9,10,11]. Chest CT and transthoracic echocardiography are indispensable diagnostic tools for identifying intracardiac cement emboli. Since pulmonary cement embolism is usually asymptomatic and the emboli are typically small, routine postoperative imaging has not been commonly recommended after PKP [12]. However, our case underscores the importance of routine postoperative chest X-ray or CT to effectively rule out intracardiac bone cement embolism.

Given the rarity of intracardiac bone cement embolism, no standardized management protocol currently exists. For asymptomatic patients, anticoagulation therapy for 3–6 months is generally recommended to allow endothelialization of the cement fragment, thereby reducing thrombogenic risk [2]. Symptomatic cases, often necessitate surgical removal or percutaneous retrieval [2, 13], but the specific approach requires a comprehensive consideration of the shape and size of the cement, and patients’ age and tolerance to the surgery. Surgical treatment is typically favored for large, sharp, or life-threatening emboli causing structural damage, such as ventricular perforation or valve destruction. Transcatheter retrieval may be a viable option for high-risk surgical candidates, particularly for emboli located in the right atrium. However, this approach is less suitable for long or sharp cement fragments, given the brittleness of bone cement and its tendency to fracture during retrieval [13]. Nonetheless, successful endovascular retrieval has been reported in select cases [10, 14]. Additionally, Pan et al. believe that cement fragments migrating to distal subsegmental pulmonary arteries are not expected to be thrombogenic [14]. In our case, a long and slender bone cement embolus traversed the tricuspid annulus and penetrated the right ventricle. Despite this, fatal pericardial tamponade did not occur due to thrombosis sealing the perforation site. Emergency surgical intervention was imperative and yielded excellent outcomes, as demonstrated in this and prior reports.

In conclusion, although rare, symptomatic intracardiac bone cement embolism represents a serious and potentially fatal complication of PKP. Rapid diagnosis and timely intervention tailored to the characteristics of the embolus and the patient’s clinical condition are essential for optimal outcomes.