Kummel Disease

Key Words

Kummel, Osteonecrosis, Vacuum Cleft, Osteoporosis, Vertebroplasty

Introduction

Kummel disease was first described by Hermann Kummell in 1891 as delayed posttraumatic vertebral collapse occurring weeks or months after an often minimal injury. The mechanism is still debated. These lesions are most widely believed to be secondary to delayed osteonecrosis of the vertebral body, potentially related to vascular disruption of the anterior watershed territory of the vertebral body following trauma. It is a rarely reported entity, which likely occurs more frequently than recognized. Typically, only one vertebral level is involved within the lower thoracic or upper lumbar spine. Kummel disease most commonly affects middle-age or elderly patients. Unlike the more commonly seen osteoporotic compression fracture, delayed vertebral osteonecrosis (Kummel disease) has a typical clinical and radiographic course. The imaging finding of the “intravertebral vacuum cleft” ( Fig. 25.1 ) has been described on plain film, computed tomography (CT), and magnetic resonance (MR) imaging. Although vertebral clefts are often associated with Kummel disease, the finding is not exclusive to this disease process.

Stages of Evolution: Overview

Initial imaging in patients that develop Kummel disease is classically radiographically occult. This is one of the defining clinical features of the entity. However, many patients who develop Kummel disease are not imaged at the time of initial injury, typically due to the minor severity of the trauma, such as a fall from standing.

Following an asymptomatic period or sometimes minor persistent pain, the patient will experience worsening of pain severity, typically greater than after the initial pain episode with or without neurologic symptoms, such as radiculopathy or bowel/bladder dysfunction.

Imaging at this delayed time point will demonstrate either a vertebral compression deformity or intravertebral “cleft” dependent upon patient positioning during imaging, weight-bearing versus supine. This is the result of a potentially dynamic (unstable) cavity that has developed within the vertebrae. Flexion or weight-bearing radiographs may demonstrate vertebral compression, while extension or supine radiographs may demonstrate a “cleft.” Nitrogen-predominant gas may fill the cleft because of the lower pressure within the cavity causing the radiographically described “intravertebral vacuum cleft” (IVC). Although IVC was initially attributed to Kummel disease, this sign has proven not to be specific to this disease process. Other conditions with IVC include intravertebral disc herniations, subacute fractures that violate the vertebral endplate, and even pathologic compression fractures.

IVCs are easily identified on CT; however, they may create confusion or misinterpretation on MRI. On MRI, one might expect hypointense signal related to the trapped gas. However, more typically T2 hyperintense fluid will fill the cavity due to prolonged supine positioning required for MRI allowing time for fluid accumulation. T1 signal is variable, as it depends on the protein concentration of the fluid. There may be an associated “double line sign” in the adjacent vertebral marrow, similar to the appearance of osteonecrosis at other sites (such as the femoral head). This finding likely represents a sclerotic rim with adjacent reactive bone surrounding the cavity.

The five clinical stages are summarized in Box 25.1 and morphologic changes to the vertebral body depicted in Fig. 25.2 .

Box 25.1

Five Clinical Stages of Kummel Disease

1.

Initial injury: Often minimal trauma or trauma ranging from mild to severe. (Imaging typically not performed, although normal if performed.)
2.

Posttraumatic period: Characterized by minimal or minor residual back pain without loss of function (continuation of activities of daily living).
3.

Variable latent stage: Patient usually feels well, although minor symptoms may be present.
4.

Recrudescent stage: Characterized by increasingly severe back pain. (Imaging at this stage will show vertebral abnormalities of vertebral collapse or an air or fluid cleft depending on patient positioning, i.e., flexion or extention/supine. See Fig. 25.2 .)
5.

Terminal stage: Vertebral body collapse and kyphosis with potential for neurologic deficit due to instability and spinal canal compromise, if untreated.