28.1 Introduction

Depending upon the duration of fractures, all vertebral fractures can be defined as acute (<6 weeks), subacute (6–24 weeks), and chronic (>24 weeks). ¹ The pathophysiology behind unhealed chronic, longer-lasting pain in these patients is multifactorial, including structural changes, nonunions, fibrous unions, osteoarthritis, and nerve irritation that results in chronic radiculopathy or complex regional pain syndrome. ² In the early era of vertebral augmentation, treating older fractures was controversial; however, numerous literature publications have proven efficacy of cement injection in these unhealed fractures as well. ^{3 – 6} According to international reporting standards both painful chronic traumatic fracture with nonunion or internal cystic changes and painful fractures associated with osteonecrosis are included in the indications of vertebral augmentation. ^{7 , 8}

28.2 Preoperative Evaluation

Preoperative imaging evaluation is a pre-requisite in chronic cases as well. Radiographs of the spine in anteroposterior and lateral projections can provide initial information concerning the number and the extent of vertebral collapse, but defining the levels of treatment by standard radiographs is inaccurate in both acute and chronic lesions. ^{2 , 9} Similarly, in chronic vertebral fractures the usefulness of scintigraphy is controversial. ² On the other hand, MRI is governed by high sensitivity for bone marrow edema indicating osseous activity at the fracture site, irrespective of the fracture’s age. Timing of the fracture (acute or chronic) should not be confused with the presence of bone edema in short TI inversion recovery (STIR) sequence of MR examination. Both acute and unhealed chronic fractures can show bone edema (illustrated as increased signal intensity on the STIR sequence) as a sign of bone marrow activity. MRI with STIR and T1-weighted sequences should be used to verify the fracture’s age and healing status (acute vs. chronic, incompletely healed vs. consolidated) (▶Fig. 28.1). ⁸ Tanigawa et al reported that the improvement after vertebral augmentation is related to the bone edema pattern illustrated in the pretherapeutic MRI (▶Fig. 28.2). Specifically according to this study patients with an extensive bone marrow edema pattern involving more than 50% of the vertebral body reported significantly greater clinical improvement than those without this pattern ¹⁰ (▶Fig. 28.3).

28.3 Vertebral Osteonecrosis

Vertebral body osteonecrosis is characterized by cellular death and bone resorption that result in mechanical insufficiency and vertebral collapse (▶Fig. 28.4). It can be idiopathic or secondary to trauma, cytotoxicity, and genetic factors. ^{11 – 13} The process of osteonecrosis and subsequent rapid collapse of a vertebral body has been given the eponymous name Kummell disease after the German surgeon Hermann Kummell who first described this condition in 1891. The pathognomonic sign of vertebral osteonecrosis is the intravertebral vacuum sign that may contain gas, fluid, or both. ¹³ MRI cannot easily distinguish between gas and compact bone, as both appear as low signal intensity areas. In case of suspicion of a gas pocket, CT imaging can easily detect the osteonecrotic gas cavity (▶Fig. 28.5). The literature examination of vertebral osteonecrosis is limited and inconsistent with substantial overlap with cases of nonunion, fibrous union, and pseudoarthrosis. ¹⁴ The most common reported risk factors include low bone density and the use of glucocorticoids but many factors may work in combination. Recently, vertebral osteonecrosis was classified into four stages based upon radiological findings and sagittal alignment: ¹³

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  0: Theoretical phase.

  
  
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  1: Early phase.

  
  
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  2: Instability phase.

  
  
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  3: Fixed deformity phase.

According to this classification proposed by Formica et al, stage 1 is managed with nonsurgical management (NSM) as opposed to stages 2 and 3 which require different therapeutic approaches according to local and global sagittal alignment. ¹³ It is evident that the treatment of vertebral osteonecrosis should be adjusted according to symptoms and disability, neurological status, comorbidities, and surgical risk.