Spinal epidural hematoma is a well known complication of spinal surgery. Clinically insignificant small epidural hematomas develop in most spinal surgeries following laminectomy. However, the incidence of clinically significant postoperative spinal epidural hematomas that result in neurological deficits is extremely rare. In this report, we present a 33-year-old female patient whose spinal surgery resulted in postoperative spinal epidural hematoma. She was diagnosed with lumbar disc disease and underwent hemipartial lumbar laminectomy and discectomy. After twelve hours postoperation, her neurologic status deteriorated and cauda equina syndrome with acute spinal epidural hematoma was identified. She was immediately treated with surgical decompression and evacuation of the hematoma. The incidence of epidural hematoma after spinal surgery is rare, but very serious complication. Spinal epidural hematomas can cause significant spinal cord and cauda equina compression, requiring surgical intervention. Once diagnosed, the patient should immediately undergo emergency surgical exploration and evacuation of the hematoma.
We present a rare case of delayed onset of epidural hematoma after lumbar surgery whose only presenting symptom was vesicorectal disturbance. A 68-year-old man with degenerative spinal stenosis underwent lumbar decompression and instrumented posterolateral spine fusion. The day after his discharge following an unremarkable postoperative course, he presented to the emergency room complaining of difficulty in urination. An MRI revealed an epidural fluid collection causing compression of the thecal sac. The fluid was evacuated, revealing a postoperative hematoma. After removal of the hematoma, his symptoms disappeared immediately, and his urinary function completely recovered. Most reports have characterized postoperative epidural hematoma as occurring early after operation and accompanied with neurological deficits. But it can happen even two weeks after spinal surgery with no pain. Surgeons thus may need to follow up patients for at least a few weeks because some complications, such as epidural hematomas, could take that long to manifest themselves.
A 67-year-old man with degenerative lumbar spinal stenosis and a medical history significant for coronary artery disease underwent routine lumbar surgical decompression. The objective of this study was to report a case of postoperative epidural hematoma associated with the use of emergent anticoagulation, including the dangers associated with spinal decompression and early postoperative anticoagulation.
After anticoagulation therapy for postoperative myocardial ischemia, the patient developed paresis with ascending abdominal paraesthesias. Immediate decompression of the surgical wound was carried out at the bedside. Magnetic resonance imaging revealed a massive spinal epidural hematoma extending from the middle of the cervical spine to the sacrum. Emergent cervical, thoracic, and revision lumbar laminectomy without fusion was performed to decompress the spinal canal and evacuate the hematoma.
Motor and sensory function returned to normal by 14 days postoperatively, but bowel and bladder function continued to be impaired. Postoperative radiographs showed that coronal and sagittal spinal alignment did not change significantly after extensive laminectomy.
Full anticoagulation should be avoided in the early postoperative period. In cases requiring early vigorous anticoagulation, patients should be closely monitored for changes in neurologic status. Combined cervical, thoracic, and lumbar laminectomy, without instrumentation or fusion, is an acceptable treatment option.
Spinal stenosis, lumbar; Spinal decompression; Anticoagulation; Epidural hematoma; Laminectomy
Traumatic cervical spinal cord injury with subaxial fracture and dislocation not only indicates a highly unstable spine but can also induce life-threatening complications. This makes first aid critically important before any definitive operative procedure is undertaken. The present study analyzes the various first aid measures and operative procedures for such injury.
Materials and Methods:
Two hundred and ninety-five patients suffered from cervical spinal cord injury with fracture and dislocation. The average period between injury and admission was 4.5 days (range 5 h-12 weeks). The injury includes burst fractures (n = 90), compression fractures with herniated discs (n = 50), fractures and dislocation (n = 88) and pure dislocation (n = 36). Other injuries including developmental spinal canal stenosis and/or multi-segment spinal cord compression associated with trauma (n = 12), lamina fractures compressing the spinal cord (n = 6), ligament injuries (n = 7) and hematoma (n = 6) were observed in the present study. The injury level was C4 (n = 17), C5 (n = 29), C6 (n = 39), C7 (n = 35), C4-5 (n = 38), C5-6 (n = 58), C6-7 (n = 49), C4-6 (n = 16) and C5-7 (n = 14). According to the Frankel grading system, grade A was observed in 20 cases, grade B in 91, grade C in 124 and grade D in 60. One hundred and eighteen (40%) patients had a high fever and difficulty in breathing on presentation. First aid measures included early reduction and immobilization of the injured cervical spine, controlling the temperature, breathing support, and administration of high-dose methylprednisolone within eight hours of the injury (n = 12) and administration of dehydration and neurotrophy medicine. Oxygen support was given and tracheotomy was performed for patients with serious difficulty in breathing. Measures were taken to prevent bedsores and infections of the respiratory and urological systems. Two hundred and thirty six patients were treated with anterior decompression, 31 patients were treated by posterior approach surgery and combined anterior and posterior approach surgery was performed in a single sitting on 28 patients.
All patients were followed for 0.5-18 years (mean 11.8 years). At least one Frankel grade improvement was observed in 178 (60.3%) patients. In the anterior surgery group, the best results were observed in the cases with slight compressive fracture with disc herniation (44/50 patients, 88.0%). In the posterior surgery group, one Frankel grade improvement was observed in the cases with developmental spinal canal stenosis with trauma, lamina fractures, ligament injuries and hematoma (27/31, 87.1%). Most of the patients in the Frankel D group recovered normal neurological function after surgery. The majority of the patients with Frankel C neurological deficit (102/124) had the ability to walk postoperatively, while most of the seriously injured patients (Frankel A and B) had no improvement in their neurological function. Radiolographic fusion of the operated segments occurred in most patients within three months. Loss of intervertebral height and cervical physiological curvature was observed to varying degrees in 30.1% (71/236) of the cases in the anterior surgery group.
First aid measures of early closed reduction or realignment and immobilization of the cervical spine, breathing support and high-dose methylprednisolone were most important in the treatment for traumatic spinal cord injury. Surgery should be performed as soon as the indications of spinal injury appear. The choice of the approach—anterior, posterior or both, should be based on the type of the injury and the surgeon's experience. Any complications should be actively prevented and treated.
Cervical spine; first aid; spinal cord injury; surgical treatment
In the surgical treatment of thoracolumbar fractures, the major problem after posterior correction and transpedicular instrumentation is failure to support the anterior spinal column, leading to loss of correction and instrumentation failure with associated complaints. We conducted this prospective study to evaluate the outcome of the treatment of acute thoracolumbar burst fractures by transpedicular balloon kyphoplasty, grafting with calcium phosphate cement and short pedicle screw fixation plus fusion.
Materials and Methods:
Twenty-three consecutive patients of thoracolumbar (T9 to L4) burst fracture with or without neurologic deficit with an average age of 43 years, were included in this prospective study. Twenty-one from the 23 patients had single burst fracture while the remaining two patients had a burst fracture and additionally an adjacent A1-type fracture. On admission six (26%) out of 23 patients had neurological deficit (five incomplete, one complete). Bilateral transpedicular balloon kyphoplasty with liquid calcium phosphate to reduce segmental kyphosis and restore vertebral body height and short (three vertebrae) pedicle screw instrumentation with posterolateral fusion was performed. Gardner kyphosis angle, anterior and posterior vertebral body height ratio and spinal canal encroachment were calculated pre- to postoperatively.
All 23 patients were operated within two days after admission and were followed for at least 12 months after index surgery. Operating time and blood loss averaged 45 min and 60 cc respectively. The five patients with incomplete neurological lesions improved by at least one ASIA grade, while no neurological deterioration was observed in any case. The VAS and SF-36 (Role physical and Bodily pain domains) were significantly improved postoperatively. Overall sagittal alignment was improved from an average preoperative 16° to one degree kyphosis at final followup observation. The anterior vertebral body height ratio improved from 0.6 preoperatively to 0.9 (P<0.001) postoperatively, while posterior vertebral body height improved from 0.95 to 1 (P<0.01). Spinal canal encroachment was reduced from an average 32% preoperatively to 20% postoperatively. Cement leakage was observed in four cases (three anterior to vertebral body and one into the disc without sequalae). In the last CT evaluation, there was a continuity between calcium phosphate and cancellous vertebral body bone. Posterolateral radiological fusion was achieved within six months after index operation. There was no instrumentation failure or measurable loss of sagittal curve and vertebral height correction in any group of patients.
Balloon kyphoplasty with calcium phosphate cement secured with posterior short fixation in the thoracolumbar spine provided excellent immediate reduction of posttraumatic segmental kyphosis and significant spinal canal clearance and restored vertebral body height in the fracture level.
Balloon kyphoplasty; calcium phosphate; neurological deficit; pedicle screw; short internal fixation; thoracolumbar vertebral fracture; transpedicular grafting
Osteoporosis is the most common contributing factor of spinal fractures, which characteristically are not generally known to produce spinal cord compression symptoms. Recently, an increasing number of medical reports have implicated osteoporotic fractures as a cause of serious neurological deficit and painful disabling spinal deformities. This has been corroborated by the present authors as well. These complications are only amenable to surgical management, requiring instrumentation. Instrumenting an osteoporotic spine, although a challenging task, can be accomplished if certain guidelines for surgical techniques are respected. Neurological deficits respond equally well to an anterior or posterior decompression, provided this is coupled with multisegmental fixation of the construct. With the steady increase in the elderly population, it is anticipated that the spine surgeon will face serious complications of osteoporotic spines more frequently. With regard to surgery, however, excellent correction of deformities can be achieved, by combining anterior and posterior approaches. Paget's disease of bone (PD) is a non-hormonal osteometabolic disorder and the spine is the second most commonly affected site. About one-third of patients with spinal involvement exhibit symptoms of clinical stenosis. In only 12–24% of patients with PD of the spine is back pain attributed solely to PD, while in the majority of patients, back pain is either arthritic in nature or a combination of a pagetic process and coexisting arthritis. In this context, one must be certain before attributing low back pain to PD exclusively, and antipagetic medical treatment alone may be ineffective. Neural element dysfunction may be attributed to compressive myelopathy by pagetic bone overgrowth, pagetic intraspinal soft tissue overgrowth, ossification of epidural fat, platybasia, spontaneous bleeding, sarcomatous degeneration and vertebral fracture or subluxation. Neural dysfunction can also result from spinal ischemia when blood is diverted by the so-called "arterial steal syndrome". Because the effectiveness of pharmacologic treatment for pagetic spinal stenosis has been clearly demonstrated, surgical decompression should only be instituted after failure of antipagetic medical treatment. Surgery is indicated as a primary treatment when neural compression is secondary to pathologic fractures, dislocations, spontaneous epidural hematoma, syringomyelia, platybasia, or sarcomatous transformation. Five classes of drugs are available for the treatment of PD. Bisphosphonates are the most popular antipagetic drug and several forms have been investigated.
Osteoporosis; Fractures; Neurological deficit; Deformity; Paget's disease; Back pain; Spinal stenosis; Myelopathy; Treatment
Although extravasations of polymethylmetharylate during percutaneous vertebroplasty are usually of little clinical consequence, surgical decompression is occasionally required if resultant neurologic deficits are severe. Surgical removal of epidural polymethylmetharylate is usually necessary to achieve good neurologic recovery. Because mobilizing the squeezed spinal cord in a compromised canal can cause further deterioration, attempts to remove epidural polymethylmetharylate in the thoracic region need special consideration. A 66-year-old man had incomplete paraparesis and radicular pain on the chest wall after percutaneous vertebroplasty for osteoporotic compression fracture of T7. Radiological studies revealed polymethylmetharylate extravasations into the right lateral aspect of spinal canal that caused marked encroachment of the thecal sac and right neuroforamina. Progressive neurologic deficit and poor responses to medical managements were observed; therefore, surgical decompression was performed 4 months later. After laminectomy and removal of facet joints and T7 pedicle on the affected side, extravasated polymethylmetharylate posterior and anterior to the thecal sac was completely removed without retracting the dura mater. Spinal stability was reconstructed by supplemental spinal instrumentation and intertransverse arthrodesis with banked cancellous allografts. Myelopathy and radicular pain gradually resolved after decompression surgery. The patient was free of sensory abnormality and regained satisfactory ambulation two years after surgical decompression.
Vertebroplasty; Polymethylmethacrylate; Epidural extravasations; Thoracic myelopathy; Surgical removal
Although postoperative spinal epidural hematoma (SEH) is not uncommon, hematomas that require surgery are rare. Cauda equina syndrome (CES) may be associated with postoperative SEH. In these cases, early recognition and emergency decompression can prevent further damage and better neurologic recovery.
A 41-year-old man underwent two-level discectomy with insertion of an interspinous spacer at L3-4 and L4-5 because of low back pain and radiculopathy. Eight hours after the operation, the patient developed CES. MRI revealed SEH compressing posteriorly at the L3-4 level. On emergency decompression and hematoma evacuation, the interspinous spacer had obstructed the laminotomy site at L3-4 completely, blocking drainage to the drain. The patient experienced complete neurologic recovery by 2 months followup.
Many studies report risk factors for SEH. However, postoperative SEH can also be encountered in patients without these risks. One study reported a critical ratio (preoperative versus postoperative cross-sectional area) correlated with postoperative symptoms, especially in those with CES. The propensity to develop CES is likely dependent on a number of patient-specific factors.
Surgeons should be aware that patients without risk factors may develop acute CES. Wider laminotomy (larger than half of the device size) may help to prevent this complication when one uses the compressible type of device, especially in patients with relatively small lamina.
To examine disc degeneration at levels adjacent and next adjacent to the fractured vertebra and to analyses, if the disc degeneration is determined by the endplate fracture.
Summary of background data
Thoracolumbar burst fracture is one of the most common spinal injuries. The diagnostic (clinical and imaging) approach and treatment of a fractured vertebra is well established; however, some controversy remains. The associated disc degeneration is less well known after 9–12 months of the short segment pedicle screw fixations. There is a major controversy whether spinal trauma with vertebral endplate fractures can result in posttraumatic disc degeneration. No study to date, however, has assessed disc degeneration of the AO type A3 thoracolumbar fractures without neurologic deficits after pedicle screw fixations.
Twenty-six patients with single-level AO type A3 thoracolumbar fractures and no neurological deficit were treated by using postural reduction and short segment percutaneous pedicle screw fixation. No laminectomy and fusion were performed. Implants were removed 9–12 months after the first operation. The thoracolumbar magnetic resonance imaging (MRI) was used to assess disc degeneration at levels adjacent and next adjacent to the fractured vertebra before the first operation and after the second operation in a retrospective study.
After the instrumentation removal, new disc degeneration was usually found at level adjacent to the cranial endplate of fractured vertebra by MRI examination in 24 patients. The average Pfirrmann grade of degenerative discs adjacent to the cranial fractured endplates deteriorated from 2.1 pre-operatively to 3.4 after the second operation. No change of disc degeneration was seen at the caudal disc space adjacent to the fractured vertebra and the levels next adjacent to the fractured vertebra. The discs next adjacent to the fractured vertebra were showed to be relatively normal without changes of degeneration during the study period.
Disc degeneration usually occurs at level adjacent to the fractured endplate of thoracolumbar burst fractures. Endplate fracture is strongly associated with disc degeneration. No correlation between fixation level and disc degeneration is seen in this study.
Disc degeneration; Thoracolumbar fracture; Endplate; Pedicle screw fixation; Minimally invasive surgery
Spinal epidural hematoma (SEH) represents the most frequent entity of acute or chronic spinal bleeding. Based upon pathogenesis, SEH can be classified as idiopathic, spontaneous, and secondary. The idiopathic forms are considered not to be attributed to any specific risk factors. Spontaneous SEH, accounting for 0.3–0.9% of all spinal epidural space occupying lesions, instead is associated with risk factors (such as substantial soft trauma or coagulation abnormalities). The chronic form, as our literature review revealed, is the rarest and its most frequent location is the lumbar spine. The pathophysiology of spontaneous and idiopathic SEH is still under debate: There are only a few reports in literature of chronically evolving SEH with progressively increasing pain and neurological impairment. Magnetic resonance imaging may be inconclusive for differential diagnosis. Here, we present two cases of lumbar chronic SEH with slow, progressive, and persistent lumbar radicular impairment. The first patient reported a minor trauma with slight back contusion and thus was classified as spontaneous SEH. In the second case not even a minor trauma was involved, so we considered it to be idiopathic SEH. In both cases preoperative blood and coagulation tests were normal and we did not find any other or co-factors in the patients’ clinical histories. MR imaging showed uncertain spinal canal obstructing lesions at L3 and L4 level in both cases. Surgical treatment allowed a correct diagnosis and resulted in full clinical and neuroradiological recovery after 1 year follow-up. Our aim is to discuss pathogenesis, clinical and radiological features, differential diagnosis and treatment options, on the background of relevant literature review.
Spontaneous; Idiopathic; Chronic; Hematoma; Epidural; Spinal
We report a series of epidural hematomas which cause neurologic deterioration after spinal surgery, and have taken risk factors and prognostic factors into consideration. We retrospectively reviewed the database of 3720 cases of spine operation in a single institute over 7 years (1998 April-2005 July). Nine patients who demonstrated neurologic deterioration after surgery and required surgical decompression were identified. Factors postulated to increase the postoperative epidural hematoma and to improve neurologic outcome were investigated. The incidence of postoperative epidural hematoma was 0.24%. Operation sites were cervical 3 cases, thoracic 2 cases, and lumbar 4 cases. Their original diagnoses were tumor 3 cases, cervical stenosis 2 cases, lumbar stenosis 3 cases and herniated lumbar disc 1case. The symptoms of epidural hematomas were neurologic deterioration and pain. After decompression, clinical outcome revealed complete recovery in 3 cases (33.3%), incomplete recovery in 5 cases (55.6%) and no change in 1 case (11.1%). Factors increasing the risk of postoperative epidural hematoma were coagulopathy from medical illness or anticoagulation therapy (4 cases, 44.4%) and highly vascularized tumor (3 cases, 33.3%). The time interval to evacuation of complete recovery group (29.3 hours) was shorter than incomplete recovery group (66.3 hours). Patients with coagulopathy and highly vascularized tumor were more vulnerable to spinal epidural hematoma. The postoperative outcome was related to the preoperative neurological deficit and the time interval to the decompression.
Clinical outcome; risk factor; postoperative; spinal epidural hematoma; spine surgery
The objective of this article is to report a case of a patient with ankylosing spondylitis who sustained a fracture through a prior solid arthrodesis without loosening or changing posterior instrumentation. There have been few cases reported of a patient with ankylosing spondylitis suffering a fracture through a prior instrumented arthrodesis. None have noted the instrumentation remaining intact with the fracture through the middle of the construct. The surgeon must be aware of this possibility to avoid spinal instability that may lead to a neurological deficit. We retrospectively reviewed the case. A review of the literature was performed through a PubMed search. A patient was found to have a fracture within a prior construct despite the presence of a posterior instrumentation. The mechanism of failure was a three-column spine fracture with “bending” of the rods. This patient was treated with a revision posterior/anterior instrumentation and fusion with placement of larger-diameter rods for added stiffness. Fractures through a prior instrumented arthrodesis are rare but still can occur in the ankylosing spondylitis patient. Given the higher risk of epidural hematoma and neurological compromise in this patient population, the surgeon must keep this on the differential diagnosis when treating patients with a prior instrumented arthrodesis.
ankylosing spondylitis; postoperative complication; spinal arthrodesis
Study design: A case report.
Objective: To report a rare case of acute spinal subdural hematoma (SSH) complicating lumbar spine surgery, its characteristic presenting symptoms, diagnostic imaging, possible cause, and pitfall in management.
Methods: A 59-year-old woman with lumbar spinal instability and stenosis underwent laminectomy and decompression at L3–L5 with instrumentation and fusion from L3–S1.
Results: Immediately following surgery, the patient presented with incapacitating pain of both lower extremities from the mid-thigh downward, which was not relieved by narcotic analgesia and was disproportional to surgical trauma. Left ankle and great toes weakness was detected at postoperative day 2 and deteriorated on day 6. Magnetic resonance imaging was performed urgently and revealed a characteristic SSH with thecal sac compression at the level of L2, proximal to the laminectomy. Emergency decompression and evacuation of the hematoma was performed. The patient had partial recovery 6 weeks postoperatively.
Conclusion: Acute SSH is a rare complication of lumbar spine surgery. This diagnosis must be considered when severe leg pain, unresolved with analgesia and disproportional to surgical trauma, with neurological deterioration occurring after lumbar spine surgery. Magnetic resonance imaging is the imaging modality of choice to assist in the differential diagnosis of an SSH. Early surgical decompression is necessary for optimal neurological recovery.
Intracranial hemorrhage is a serious but rare complication of spinal surgery, which can occur in the intracerebral, cerebellar, epidural, or subdural compartment.
To describe patients with intracranial hemorrhage after lumbar spinal surgery and present clinical and diagnostic imaging findings.
In this retrospective study, medical records of 1,077 patients who underwent lumbar spinal surgery in our tertiary referral neurosurgery center between January 2003 and September 2010 were studied. The original presentations of the patients before the surgical intervention were herniated lumbar disc, spinal canal stenosis, spondylolisthesis, lumbar spinal trauma, and lumbar spine and epidural tumor. The operations performed consisted of discectomy, multiple level laminectomy, stabilization and fusion, lumbar instrumentation, and lumbar spinal and epidural tumor resection.
Four cases developed intracranial hemorrhage including acute subdural hematoma (one case), epidural hematoma (one case), and remote cerebellar hemorrhage (two cases). The clinical and diagnostic imaging characteristics along with treatments performed and outcomes of these four patients are described and the pertinent literature regarding post-lumbar spinal surgery intracranial hemorrhages is reviewed.
Though rare, intracranial hemorrhage can occur following lumbar spinal surgery. This complication may be asymptomatic or manifest with intense headache at early stages any time during the first week after surgery. Dural tear, bloody CSF leakage, focal neurologic symptoms, and headache are indicators of potential intracranial hemorrhage, which should be considered during or following surgery and necessitate diagnostic imaging.
Intracranial hemorrhage; Lumbar spine surgery; Remote cerebellar hemorrhage; Subdural hematoma; Epidural hematoma
Spinal subarachnoid hemorrhages (SAH) can extend into the intracranial subarachnoid space, but, severe cerebral vasospasm is rare complication of the extension of intracranial SAH from a spinal subarachnoid hematoma. A 67-year-old woman started anticoagulant therapy for unstable angina. The next day, she developed severe back pain and paraplegia. MRI showed intradural and extramedullar low signal intensity at the T2-3, consistent with intradural hematoma. High signal intensity was also noted in the spinal cord from C5 to T4. We removed subarachnoid hematoma compressing the spinal cord. The following day, the patient complained of severe headache. Brain CT revealed SAH around both parietal lobes. Three days later, her consciousness decreased and left hemiplegia also developed. Brain MRI demonstrated multiple cerebral infarctions, mainly in the right posterior cerebral artery territory, left parietal lobe and right watershed area. Conventional cerebral angiography confirmed diffuse severe vasospasm of the cerebral arteries. After intensive care for a month, the patient was transferred to the rehabilitation department. After 6 months, neurologic deterioration improved partially. We speculate that surgeons should anticipate possible delayed neurological complications due to cerebral vasospasm if intracranial SAH is detected after spinal subarachnoid hematoma.
Spinal subarachnoid hematoma; Intracranial subarachnoid hemorrhage; Vasospasm; Cerebral infarction
Postoperative spinal extradural hematomas are rare. Most of the cases that have been reported occured within 3 days of surgery. Their occurrence in a delayed form, that is, more than 72 hours after surgery, is very rare. This case is being reported to enhance awareness of delayed postoperative spinal extradural hematomas.
We report a case of acute onset dorsal spinal extradural hematoma from a paraspinal muscular arterial bleed, producing paraplegia 72 hours following surgery for excision of a spinal cord tumor at T8 level. The triggering mechanism was an episode of violent twisting movement by the patient. Fresh blood in the postoperative drain tube provided suspicion of this complication. Emergency evacuation of the clot helped in regaining normal motor and sensory function. The need to avoid straining of the paraspinal muscles in the postoperative period is emphasized.
Most cases of postoperative spinal extradural hematomas occur as a result of venous bleeding. However, an arterial source of bleeding from paraspinal muscular branches causing extradural hematoma and subsequent neurological deficit is underreported. Undue straining of paraspinal muscles in the postoperative period after major spinal surgery should be avoided for at least a few days.
This is a retrospective study of 76 children who had had malignant tumours treated with laminectomy or laminoplasty and/or radiation therapy affecting the spine. Spinal tumours in children are extremely rare. However, their treatment can result in progressive spinal deformity. Radiation therapy affecting the growing spine can lead to asymmetric vertebral growth, causing kyphosis and/or scoliosis. These spinal deformities pose one of the most challenging problems for the spine surgeon. The aim of this article is to describe late-onset post-laminectomy/post-radiation spinal deformities and to evaluate the results of their treatment. Seventy-six children, with a mean age of 4 years and 7 months (range, 2 months to 16 years), underwent surgical removal of malignant tumours, between 1961 and 1995. Sixty-seven of them developed post-laminectomy/post-radiation spinal deformity. Conservative treatment consisted of bracing and corrective plaster casts. In 46 cases the deformity was treated surgically. A distraction plaster cast was used as preoperative preparation in the more severe and rigid curves, with or without neurological impairment. Surgery consisted of combined anterior and posterior fusion in 39 cases and posterior fusion in seven cases. Posterior instrumentation was used in 38 cases. The mean follow-up period was 6 years and 7 months (range, 9 months to 20 years and 2 months). Nine children did not develop deformity following the primary tumour treatment. One of them underwent laminectomy with posterolateral fusion and eight had laminoplasty combined with external immobilisation. Forty-six children developed iatrogenic kyphosis and underwent surgical correction from a mean of 75° pre-correction to a mean of 32°. The mean scoliotic angle correction was 66° preoperatively to 34° postoperatively. At follow-up, the mean correction loss was 7° in the sagittal plane and 5° in the coronal plane. Preoperative distraction plaster cast treatment resulted in a correction of 39% in kyphosis and of 58% in scoliosis, and in a partial or complete recovery of neurological deficits in all but one patient. In severe and rigid curves that develop following treatment of paediatric spinal tumours, preoperative application of a distraction plaster cast can reduce deformity and facilitate surgical correction. Furthermore, in the case of pure bony compression of the spinal cord due to the apical vertebra of the deformity, treatment with the distraction plaster can result in recovery from the neurological impairment. The prevention of post-laminectomy/post-radiation spine deformities is emphasised. Rigid external immobilisation for a period of 4 months in the cervical spine and of 6 months in the thoracic spine is recommended after both laminoplasty and laminectomy with posterolateral fusion.
Laminectomy; Laminoplasty; Radiation therapy; Spinal deformity; Spine fusion; Distraction plaster
The major problem after posterior correction and instrumentation in the treatment of thoracolumbar burst fractures is failure to support the anterior spinal column leading to loss of correction of kyphosis and hardware breakage. We conducted a prospective consecutive series to evaluate the outcome of the management of acute thoracolumbar burst fractures by transpedicular hydroxyapatite (HA) grafting following indirect reduction and pedicle screw fixation.
Materials and Methods:
Eighteen consecutive patients who had thoracolumbar burst fractures and associated incomplete neurological deficit were operatively treated within four days of admission. Following indirect reduction and pedicle screw fixation, transpedicular intracorporeal HA grafting to the fractured vertebrae was performed. Mean operative time was 125 min and mean blood loss was 150 ml. Their implants were removed within one year and were prospectively followed for at least two years.
The neurological function of all 18 patients improved by at least one ASIA grade, with nine (50%) patients demonstrating complete neurological recovery. Sagittal alignment was improved from a mean preoperative kyphosis of 17°to −2°(lordosis) by operation, but was found to have slightly deteriorated to 1° at final followup observation. The CT images demonstrated a mean spinal canal narrowing preoperatively, immediate postoperative and at final followup of 60%, 22% and 11%, respectively. There were no instances of hardware failure. No patient reported severe pain or needed daily dosages of analgesics at the final followup. The two-year postoperative MRI demonstrated an increase of one grade in disc degeneration (n = 17) at the disc above and in 11 patients below the fractured vertebra. At the final followup, flexion-extension radiographs revealed that a median range of motion was 4, 6 and 34 degrees at the cranial segment of the fractured vertebra, caudal segment and L1-S1, respectively. Bone formation by osteoconduction in HA granules was unclear, but final radiographs showed healed fractures.
Posterior indirect reduction, transpedicular HA grafting and pedicle screw fixation could prevent the development of kyphosis and should lead to reliable neurological improvement in patients with incomplete neurological deficit. This technique does not require fusion to a segment, thereby preserves thoracolumbar motion.
Pedicle screw fixation; thoracolumbar burst fracture; transpedicular hydroxyapatite grafting
A 26-year-old male who had no underlying disease, including coagulopathy, underwent thoracotomy and bleeding control due to hemothorax. On the fifth postoperative day, paralysis of both lower limbs occurred. Urgent spine magnetic resonance imaging showed a massive anterior spinal epidural hematoma from C2 to L1 level with different signal intensities, which was suspected to be staged hemorrhage. Hematoma evacuation with decompressive laminectomy was performed. The patient's neurologic deterioration was recovered immediately, and he was discharged without neurological deficits. A drug history of naftazone, which could induce a drug-induced platelet dysfunction, was revealed retrospectively. To our knowledge, this is the first report of whole spontaneous spinal epidural hematoma in a young patient, with a history of hemorrhoid medication.
Epidural hematoma; Naftazone; Spinal hematoma
Axillary artery injury in the shoulder region following blunt trauma without association with either shoulder dislocation or fracture of the humeral neck has been previously reported. Axillary artery injury might also be accompanied with brachial plexus injury. However, delayed onset of brachial plexus palsy caused by a compressive hematoma associated with axillary injury after blunt trauma in the shoulder region has been rarely reported. In previous reports, this condition only occurred in old patients with sclerotic vessels. We present a case of a young patient who suffered axillary artery injury associated with brachial plexus palsy that occurred tardily due to compressive hematoma after blunt trauma in the shoulder region without association of either shoulder dislocation or humeral neck fracture.
A 16-year-old male injured his right shoulder in a motorbike accident. On initial physical evaluation, the pulses on the radial and ulnar arteries in the affected arm were palpable. Paralysis developed later from 2 days after the injury. Functions in the right arm became significantly impaired. Angiography showed complete occlusion of the axillary artery. Magnetic resonance imaging demonstrated a mass measuring 4 × 5 cm that was suspected to be a hematoma compressing the brachial plexus in a space between the subscapular muscle and the pectoralis minor muscle. Surgery was performed on the third day after injury. In intraoperative observations, the axillary artery was occluded with thrombus along 5 cm; a subscapular artery was ruptured; the brachial plexus was compressed by the hematoma. After evacuation of the hematoma, neurolysis of the brachial plexus, and revascularization of the axillary artery, the patient had an excellent functional recovery of the affected upper limb, postoperatively.
Surgeons should be aware that axillary artery injuries may even occur in young people after severe blunt trauma in the shoulder region and can be associated with secondary brachial plexus injury due to a hematoma. For treatment in cases with progressive nervous deficit after trauma, not only reconstruction of the injured artery but also immediate evacuation of the hematoma, and exploration of the brachial plexus are necessary to avoid irreversible neurological damage.
Patients suffering from polytrauma often present with altered mental status and have varying levels of examinability. This makes evaluation difficult. Physicians are often required to rely on advanced imaging techniques to make prompt and accurate diagnoses. Occasionally, injury detection on advanced imaging studies can be challenging given the subtle findings associated with certain conditions, such as diffuse idiopathic skeletal hyperostosis (DISH). Delayed or missed diagnoses in the setting of spinal fracture can lead to catastrophic neurological injury.
A man struck by a motor vehicle suffered multiple traumatic injuries including numerous rib fractures, a mechanically unstable pelvic fracture, and also had suspicion for an aortic injury. Unfortunately, the upper thoracic segment (T1-5) was only visualized with axial images based on the electronic data. Several days later, a contrast CT scan obtained to check the status of suspected aortic injury revealed T3-T4 subluxation indicative of an unstable extension-type fracture in the setting of DISH. Due to the missed injury and delay in diagnosis, surgery was not performed until eight days after the injury. At surgery, the patient was found to have left T3-T4 facet joint infection as well as infected hematoma surrounding a left T4 transverse process fracture and a traumatic T4 costo-transverse joint fracture-subluxation. Despite presence of infection, an instrumented posterior spinal fusion from T1-T6 was performed and the patient recovered well after antibiotic treatment.
A T3-T4 unstable DISH extension-type fracture was initially missed in a polytrauma patient due to inadequate imaging acquisition, which caused a delay in treatment and bacterial seeding of fracture hematoma. Complete imaging is especially needed in obtunded patients that cannot be thoroughly examined.
Spinal epidural hematomas (SEHs) are rare complications following spine surgery, especially for single level lumbar discectomies. The appropriate surgical management for such cases remains to be investigated. We report a case of an extensive spinal epidural hematoma from T11-L5 following a L3-L4 discectomy. The patient underwent a single level L4. A complete evacuation of the SEH resulted in the patient's full recovery. When presenting symptoms limited to the initial surgical site reveal an extensive postoperative SEH, we propose: to tailor the surgical exposure individually based on preoperative findings of the SEH; and to begin the surgical exposure with a limited laminectomy focused on the symptomatic levels that may allow an efficient evacuation of the SEH instead of a systematic extensive laminectomy based on imaging.
Epidural; Hematoma; Spine; Surgery; Management; Emergency; Postoperative
We present the results of the treatment of infected primary or delayed spine wounds after spinal surgery using negative pressure wound therapy. In our institution (University Hospital Zurich, Switzerland) nine patients (three women and six men; mean age 68.6, range 43-87 years) were treated in the period between January to December 2011 for non-healing spinal wounds. The treatment consisted of repeated debridements, irrigation and temporary closure with negative pressure wound therapy system. Three patients were admitted with a spinal epidural abscess; two with osteoporotic lumbar fracture; two with pathologic vertebra fracture and spinal cord compression, and two with vertebra fracture after trauma. All nine patients have been treated with antibiotic therapy. In one case the hardware has been removed, in three patients laminectomy was performed without instrumentation, in five patients there was no need to remove the hardware. The average hospital stay was 16.6 days (range 11-30). The average follow-up was 3.8, range 0.5-14 months. The average number of negative pressure wound therapy procedures was three, with the range 1-11. Our retrospective study focuses on the clinical problems faced by the spinal surgeon, clinical outcomes after spinal surgery followed by wound infection, and negative pressure wound therapy. Moreover, we would like to emphasize the importance for the patients and their relatives to be fully informed about the increased complications of surgery and about the limitations of treatment of these wounds with negative pressure wound therapy.
spinal infections; vacuum assisted therapy; infection; spinal surgery
Subfascial wound suction drains are commonly used after spinal surgery to decrease the incidence of post-operative hematoma. However, there is a paucity of literature regarding their effectiveness.
To report four cases of post-operative spinal epidural hematoma causing massive neurological deficit in patients who had subfascial suction wound drains.
During an 8-year period, a retrospective review of 1750 consecutive adult spinal surgery cases was performed to determine the incidence, commonalities, and outcomes of catastrophic neurological deficit caused by post-operative spinal epidural hematoma.
Epidural hematoma causing major neurological deficit (American Spinal Injury Association B) was identified in 4 out of 1750 patients (0.23%). All four patients in this series had subfascial wound suction drains placed prophylactically at the conclusion of their initial procedure.
Three patients developed massive neurological deficits with the drain in place; one patient had the drain removed at 24 hours and subsequently developed neurological symptoms during the following post-operative day. Significant risk factors for the development of hematoma were identified in two of the four patients. Average time to return to the operating room for hematoma evacuation was 6 hours (range 3–12 hours). Neurological status significantly improved in all four patients after hematoma evacuation.
Post-operative epidural hematoma causing catastrophic neurological deficit is a rare complication after spinal surgery. The presence of suction wound drains does not appear to prevent the occurrence of this devastating complication.
Epidural hematoma; Suction drainage; Spinal cord injuries; Laminectomy; Spinal decompression
Intraspinal bleeding especially in the form of subdural hematoma is rare in hemophiliacs. In the present case, we report a neglected hemophilic A child with such a problem and discuss its management options.
A 9-year old hemophilic A boy presented with quadriparesis, confusion and meningismus after a fall 4 days previously. There was no sign of direct trauma to his back. His CT Scan and MRI showed spinal extramedullary hematoma extended from C5 to L2. We corrected the factor VIII level, but two days later, the patient's lower limbs weakened to 1/5 proximally as well as distally. We performed a laminectomy from T11 to L2, according to the level of the maximal neurological deficit and recent deterioration course. The subdural hematoma was evacuated. The hematoma in other spinal levels was managed conservatively. In the week following the operation, the patient's neurological status approached normal.
This case calls attention to the clinical manifestation, radiological features and management options of the rarely reported intraspinal hematoma in hemophilic children. Although this case has been managed operatively for its hematoma in the thoracolumbar region, at the same time it can be considered a successful case of conservative management of intraspinal hematoma in the cervicothoracic region. Both conservative and surgical management could be an option in managing these patients considering their neurological course.
Hematoma; Hemophilia; Spine; Subdural.