Journal of Spine & NeurosurgeryISSN: 2325-9701

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Case Report, J Spine Neurosurg Vol: 2 Issue: 4

A Case of Avascular Necrosis of a Lumbar Vertebral Body after Sport Injury

Mohamad Faraji Rad*, Amirshahriar Ariamanesh, Hamidreza Eghbalee and Elnaz Farajirad
Department of Neurosurgery, Mashad University of Medical sciences, Mashad, Iran
Corresponding author : Mohamad Faraji Rad
Mashad University of Medical Sciences 48 Mollasadra 4 Ahmadabad BLVD Mashad 9176563378, Iran
E-mail: [email protected]
Received: December 12, 2012 Accepted: August 29, 2013 Published: Spetember 04, 2013
Citation: Rad MF, Ariamanesh A, Eghbalee H, Farajirad E (2013) A Case of Avascular Necrosis of a Lumbar Vertebral Body after Sport Injury. J Spine
Neurosurg 2:4. doi:10.4172/2325-9701.1000119


 A Case of Avascular Necrosis of a Lumbar Vertebral Body after Sport Injury

Avascular necrosis of vertebral body is not common. There are some radiologic findings that imply avascular necrosis however they are not characteristic. It is due to obliteration of blood supply of bone after trauma and non traumatic events.

Keywords: Avascular necrosis; Vertebral body; Sport


Avascular necrosis; Vertebral body; Sport


Ischemic necrosis of bone like infarction in other organs is because of significant reduction or obliteration of blood supply in affected areas [1].
Vertebral osteonecrosis is a rare disease and is thought to be the consequence of an insult to anterior segment of the vertebral body, with either traumatic or non traumatic mechanism.
The first mechanism is called Kümmell disease and represents delayed vertebral collapse after major trauma [2]. The second mechanism involves repeated microtrabecular fractures in a vertebral body that is weakened because of osteoporosis, replacement of marrow by abnormal cells, or long-term administration of glucocorticoids [3]. This case report is about an avascular necrosis of the 5th lumbar vertebra after sport injury in a healthy young adult.

Case Report

A healthy 29-year-old man with no previous problem referred with severe low back pain after a sudden slip and fall in a soccer match. He experienced such a severe back pain that could not drive home that day. The pain subsided gradually but dull chronic low back pain remained after a week.
The early lumbosacral radiographs which had been taken 4 months before worsening the pain showed no pathology (Figure 1). Lumbosacral MRI was not advised because the patient was neurologically intact and plain X-Rays were normal. Evidences of osteoporosis, fracture, infiltration or congenital abnormalities were not observed.
Figure 1: Initial antero-posterior and lateral lumbosacral radiographies of the patient shows normal bone density without evidences of fracture or abnormality.
A course of medical and physical therapy was prescribed. The patient started to intake Ibuprofen 1200 mg and Baclofen 30 mg per day for two weeks. Physiotherapy exercises were performed for two weeks subsequently. During history taking, no risk factor including malnutrition, malabsorption, drug intake, drug abuse and familial diseases were observed. In general physical examination the only symptom was chronic low back pain and neurological examination was normal. Standard laboratory studies included a complete blood count, electrolyte panel, glucose, and coagulation panel which were found to be normal. The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) level were normal according to age and gender of the patient (12 and negative respectively). Metabolic studies included serum calcium (10.1 mg/dl), inorganic phosphate (3.9 mg/ dl) and 25-hydroxyvitamin D (49 ng/ml) which were normal. After a period of nearly 4 months inspite of medical therapy (included NSAIDs, rest and physical therapy) the patient still had low back pain so another lumbosacral radiography was done.
The second lumbosacral imaging showed a collapsed L5 vertebra (Figure 2). CT scan of the affected vertebra showed nonspecific areas of sclerosis and lysis in the body of L5 vertebra (Figure 3). In MRI examination no specific changes in soft tissue or thecal sac adjacent to the collapsed vertebra was not found (Figure 4). Whole body bone scan was negative for multiple or disseminated lesions (Figure 5).
Figure 2: Lateral Lumbosacral radiography of the patient after 4 months shows collapse of the 5th lumbar vertebral.
Figure 3: CT scan of the lumbosacral area shows collapse and sclerosis of the 5th lumbar vertebral body without evidence of paraspinal mass. Posterior arc is intact.
Figure 4: Lumbosacral MRI demonstrates signal change in the 5th lumbar vertebral body and vacuum cleft sign. Soft tissue is not involved and other vertebral bodies have normal shape and signal intensity.
Figure 5: Bone scan of the patient after vertebral collapse did not show multiple lesions.
We decided to take a needle biopsy specimen from L5 vertebra. Under GA and fluoroscopy guide from transcutaneus-transpedicular approach, a specimen of L5 vertebral body was obtained (Figure 6).
Figure 6: Needle biopsy of the 5th vertebrae was done to take a biopsy specimen. Under fluoroscopy guide and prone position from transcutaneustranspedicular approach we obtained bone tissue.
The pathology report emphasized that the specimen is “formed from fibro- connective and osseous tissues without any remarkable finding”. Because of chronic low back pain and onset of paresthesias in right lower limb, we decided to plan L5 corpectomy and fusion procedure. In a transperitoneal approach, corpectomy of L5 vertebra and L4-5, L5-S1 discectomy and fusion with IMPLANT® lumbar expandable cage were done (Figure 7). Anterior approach to address the anterior pathology was offered to the patient. Iliac bone of the patient was not used to avoid the graft site morbidity and also because of the patient preference.
Figure 7: Post operative lumbosacral imaging of the patient shows L5 corpectomy and anterior fusion. The operation performed via transperitoneal approach with the assistance of general surgery team. The cage is in appropriate location and spinal column maintained sagittal stability.
Pain and paresthesias subsided after procedure. Pathology report was compatible with avascular necrosis of L5 vertebral body. Biopsy Sections showed trabecular bone without osteocytes, and bone marrow showed necrotic cells (Figure 8).
Figure 8: Pathology exam is compatible with aseptic or ischemic vertebral necrosis. X=400. Section shows trabecular bone without osteocytes and bone marrow shows necrotic cells.


As previously described, ischemic necrosis of bone like infarction in other systems of body is because of a significant reduction or obliteration of the blood supply in affected areas [1]. One of the following phenomena can usually be proposed or inferred as an impending blood flow:
(1) Intraluminal obstruction (e.g: thromboembolic disorders, sludging of blood cells or stasis)
(2) Vascular compression ( e.g: external mechanical pressure or vasospasm)
(3) Physical disruption of the vessel (e.g: trauma). These factors can act alone or in combination [4].
The production of ischemic injury or necrosis and the rapidity with which cell death occurs depends on the sensitivity of the individual cell type. It is generally believed that hematopoietic elements are the first to undergo anoxic death (in 6 to 12 hours), followed by bone cells (osteocytes, osteoblasts, and osteoblasts; in 12 to 48 hours) and, subsequently, marrow fat cells (48 hours to 5 days) [5].
In 1891, Kümmel described a post traumatic osteitis in which painful kyphosis developed in several patients after a symptom-free period of months to years following an injury [6]. Subsequently, Schmorl and Janghanns [7] provided pathological observations supporting the concept of delayed post traumatic collapse of vertebral bodies, although the nature of the underlying disease process was not clear.
The prevalence of Kümmell’s disease is not known clearly, although it is probably not uncommon. The patients are generally middle –aged or elderly men or women, the interval between formations of collapse varies from days to years, and the lower thoracic and upper lumbar vertebral bodies are principally involved. Chronic back pain is a characteristic clinical finding [8].
The traumatic event might be a minor injury, and osteoporosis is not a consistent finding.
A single vertebra or more rarely multiple vertebrae are affected. Aseptic necrosis begins as a painless bone abnormality and it can remain painless. The involved bone often later becomes painful, especially in activities.
In a new study vertebral bodies at T12 and L1 were most often involved and together accounted for about two thirds of all affected vertebral bodies [4].
Conditions that are associated with aseptic necrosis include alcoholism, cortisone medications, Cushing’s syndrome, radiation exposure, Sickle cell disease, pancreatitis, gaucher disease, systemic lupus erythematosus, and malignancy [9].
Clinical presentation is typically a middle aged man with backache after trauma. Asymptomatic period is usually followed.
After weeks to months, osteonecrosis of the vertebral body predictably causes a collapse and consequently severe pain. Then, kyphotic deformity and neurologic symptoms may occur [10].
In this case, the patient had no risk factor for aseptic necrosis. He was young and not osteoporotic. He experienced a mild to moderate trauma and had pain from the beginning. The affected vertebra was unusual site for traumatic osteonecrosis. According to medical history and physical examination, the patient had no risk factor for osteoporosis. The laboratory tests were normal and plain radiographies did not suggest osteoporosis, so we did not perform bone densitometry.
MR imaging has been used to study the intravertebral vacuum phenomenon [11]. In reported cases, decreased signal intensity in the area of the vacuum cleft has been observed on T1- weighted spin echo images and hyper intensity in this region (probably reflecting the presence of fluids) has been evident on T2- weighted images [12]. However low signal intensity, probably related to the gas itself, may be seen on T2 –weighted images as well. The linear or band like pattern of abnormal signal intensity assumes diagnostic importance [13].
Gas within a vertebral body is even not diagnostic for osteonecrosis, osteoporotic fractures or neoplasm. We should differentiate between spinal infection, degenerative cysts and Shmorl’s nodes.
Collection of intravertebral fluid has been described in cases of vertebral osteonecrosis, mainly on MR imaging [14]. In a study vertebral collapse was significantly more severe in those having only intravertebral air than in those having intravertebral fluid with or without air.
Collapse was also significantly more severe when air was present than when fluid was present [15]. In our case the MRI shows low intensity signal in both T1 and T2- weighted images probably due to air in the collapsed vertebrae.
Although relatively non-specific, a bone –scan shows early activity [16].
Kummells disease is a post traumatic vertebral fracture that is initially asymptomatic and radiographically negative, but finally vertebral body collapse occurs [17]. One way to establish the diagnosis of avascular necrosis is performing spinal angiography.
Because of rare but significant side effects of angiography we decided not to perform it. Only few reports are presented which have done angiography [18]. Ideally Kummell’s disease is diagnosed on the basis of repetitive plain x-rays, in which initial films do not demonstrate evidence of a fracture [16].
Differential diagnosis includes neoplasms, chronic steroid administration, infection, osteoporosis, radiotherapy, intraosseous disc prolapse, and arteriosclerosis or alcohol abuse. Medical conditions such as pancreatitis, cirrhosis and Erdheim Chester disease also should be considered. Most of these diagnoses could be ruled out by careful history taking and physical examination. Disk herniation can be investigated with MRI study. Infection is an important differential diagnosis. It can be pyogenic or nonpyogenic (tubercular or fungal). MRI characteristics of infection and enhancement can help to differentiate infection from necrosis. Again physical exam and laboratory tests can aid in diagnosis. Sometimes, advanced spondylosis can be confused with osteonecrosis like malignancies (eg: myeloma, lymphoma) and metastasis. A definitive diagnosis can usually be established by needle biopsy in such cases.
Erdheim Chester disease should be included in the differential diagnosis in patients with lytic lesions of the spine. It is a systemic disease with a broad spectrum of clinical manifestations. Bilateral and symmetrical long bone involvement is almost universal in ECD patients. Bone pain is the most frequent symptom associated with ECD and mainly affects the lower limbs, knees and ankles. Involvement of the axial skeleton is rare, occurring almost exclusively with osteosclerosis of the extremities [19,20].
Infarcts, including those in bone, are three dimensional and can be sub- divided into four zones:
A central zone of cell death surrounded by successive zones of ischemic injury, active hyperemia and finally normal tissue [1]. Histopathology demonstrates spongiosa with multiple hemorrhages, atrophy of the bony frame work, multiple microscopic fractures, inflammatory changes and paravertebral fibrosis [10,16].


Avascular necrosis of a vertebral body without trauma is rare. This may be attributed to a wedge vertebra that causes repeated microtrauma and resulting in avascular necrosis on the adjacent vertebra due to insufficient blood supply. Surgical treatment is required in avascular necrosis of a vertebral body with progressive collapse and neurologic compromise secondary to fracture of a wedge-shaped vertebra at the lumbar region.


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