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.
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
•Spontaneous epidural hematoma of the spine (SEHS) is an extremely rare entity.•Early diagnosis and treatment showed to have the best outcome.•SESH should be suspected in every acute medullary syndrome with spinal pain, motor and/or sensory deficit.
Spontaneous epidural hematoma of the spine (SEHS) is an extremely rare entity. Patients known to have thrombophilia or on anticoagulant drugs are the most affected. It is generally caused by a rupture of the postero-internal vertebral venous plexus secondary to minor barotrauma such as cough, peridural catheter insertion...
Early diagnosis and treatment showed to have the best outcome.
We report 3 cases of spontaneous epidural hematoma in patients treated by acenocoumarol, which occurred without any provocative factor. All 3 patients were treated with decompressive laminectomy.
We described the MRI findings and discussed the spontaneity of the entity. Our present case studies and the review of the literature showed that early diagnosis and management of SEHS can lead to improvement of the neurological state and avoid definitive motor and sensitive deficit.
This rare entity should be suspected in every acute medullary syndrome with spinal pain, motor and/or sensory deficit. In order to decrease the sequelae, neurologically unstable patients should benefit from early diagnosis and urgent surgical decompression.
Spontaneous epidural hematoma of the spine; Oral anticoagulants; Acenocoumarol
We present a rare case of spinal epidural hematoma (SEH) after thoracolumbar posterior fusion without decompression surgery for a thoracic vertebral fracture. A 42-year-old man was hospitalized for a thoracic vertebral fracture caused by being sandwiched against his back on broken concrete block. Computed tomography revealed a T12 dislocation fracture of AO type B2, multiple bilateral rib fractures, and a right hemopneumothorax. Four days after the injury, in order to promote early orthostasis and to improve respiratory status, we performed thoracolumbar posterior fusion surgery without decompression; the patient had back pain but no neurological deficits. Three hours after surgery, he complained of acute pain and severe weakness of his bilateral lower extremities; with allodynia below the level of his umbilicus, postoperative SEH was diagnosed. We performed immediate revision surgery. After removal of the hematoma, his symptoms improved gradually, and he was discharged ambulatory one month after revision surgery. Through experience of this case, we should strongly consider the possibility of preexisting SEH before surgery, even in patients with no neurological deficits. We should also consider perioperative coagulopathy in patients with multiple trauma, as in this case.
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
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.
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
Spinal epidural abscess (SEA) and spinal epidural hematoma (SEH) are neurologic emergencies with distinct etiologies and treatment. Despite similarities on magnetic resonance imaging (MRI), their differentiation is usually possible with meticulous history taking and neurologic examinations. We report an unusual case of SEA that developed from preceding SEH, posing a diagnostic challenge to physicians. A 65-year-old diabetic man suddenly experienced back pain and weakness of both legs when he lifted heavy luggage. He was afebrile, and his laboratory tests were mostly unremarkable. Spinal MRI consisting of T1-weighted, T2-weighted, and fat-suppressed T2-weighted images revealed an epidural mass over the L2-L4 spinous process. He was diagnosed with SEH based on his symptoms and MRI findings, and was treated conservatively using steroid pulse therapy. Despite initial improvement, he suddenly developed into septic shock and coma on the 10th hospital day, and died shortly thereafter. An autopsy revealed massive pus accumulation in the lumbar epidural space and brain, and a postmortem diagnosis of infected SEH associated with invasive pneumococcal disease was established. Serial MRI studies, including diffusion-weighted and/or gadolinium-enhanced T1-weighted images are warranted in patients with a presumed diagnosis of SEH receiving steroid therapy to detect such infectious transformation.
Invasive pneumococcal disease; magnetic resonance imaging; spinal epidural abscess; spinal epidural hematoma
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
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
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
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
Study Design Case report.
Objectives To describe a case of delayed-onset spinal hematoma following the breakage of a spinal epidural catheter.
Methods The authors describe the clinical case review.
Results A 64-year-old woman had undergone epidural anesthesia 18 years before she was referred to our hospital because of lower-back pain and lower neurologic deficit with leg pain. The clinical examination showed the presence of a fragment of an epidural catheter in the thoracolumbar canal, as assessed by computed tomography, and a spinal hematoma that compressed the spinal cord at the same spinal level, as assessed by magnetic resonance imaging. Surgical removal of the epidural catheter and decompression surgery were performed. The patient exhibited substantial clinical improvement 1 month after surgery; she achieved a steady gait without the need for a cane and had no leg pain.
Conclusion This is the first report of delayed onset of spinal hematoma following the breakage of an epidural catheter. Generally, when the breakage of an epidural catheter occurs without symptoms, follow-up alone is recommended. However, because spinal hematoma might exhibit a late onset, the possibility of this complication should be considered when deciding whether to remove the catheter fragment. We believe that in our patient, there could be a relationship between the catheter fragment and subdural hematoma, and catheter breakage could have been a risk factor for the spinal hematoma.
epidural catheter; spinal interdural hematoma; breakage; complication
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.
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.
Spontaneous spinal epidural hematoma (SSEH) is an uncommon neurological emergency which can present with the features ranging from simple back pain with radiculopathy to complete paraplegia or quadriplegia depending on the site and severity of the compression. Spinal hemorrhage associated with anti-platelet drugs is rarely seen. We report a case of SSEH in a 68-year-old hypertensive male who was on a low dose clopidogrel for secondary stroke prophylaxis and presented with bilateral lower limb paralysis, preceeded by severe back bain. A spinal magnetic resonance imaging scan was performed which revealed a posterior epidural hematoma of the thoraco-lumbar spine. To the best of our knowledge, not more than four cases of clopidogrel related spinal epidural hematoma have been reported. Emergent decompressive laminectomy was done within 4 hours of the presentation with excellent clinical outcome. Clinicians should, therefore, consider the remote risk of SSEH in hypertensive patients who are on anti-platelet drugs as early decompressive laminectomy and evacuation of the hematoma minimizes the permanent neurological damage.
Clopidogrel; decompressive laminectomy; hypertension; spontaneous spinal epidural hematoma
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 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
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.
Spinal epidural angiolipoma is a rare benign tumor containing vascular and mature adipose elements. A slow progressive clinical course was mostly presented and rarely a fluctuating course during pregnancy. The authors report the original case of spontaneous spinal epidural bleeding resulting from thoracic epidural angiolipoma who presented with hyperacute onset of paraplegia, simulating an extradural hematoma. The patient was admitted with sudden non-traumatic hyperacute paraplegia during a prolonged walk. Neurologic examination showed sensory loss below T6 and bladder disturbances. Spinal MRI revealed a non-enhanced heterogeneous thoracic epidural lesion, extending from T2 to T3. A bilateral T2–T4 laminectomy was performed to achieve resection of a lipomatous tumor containing area of spontaneous hemorrhage. The postoperative course was uneventful with complete neurologic recovery. Histologic examination revealed the tumor as an angiolipoma. Because the prognosis after rapid surgical management of this lesion is favorable, the diagnosis of spinal angiolipoma with bleeding should be considered in the differential diagnosis of hyperacute spinal cord compression.
Angiolipoma; Epidural spinal tumor; Spinal cord compression; Spinal epidural hematoma
We report three cases of spontaneous spinal epidural hematoma (SSEH) with hemiparesis. The first patient was a 73-year-old woman who presented with left hemiparesis, neck pain, and left shoulder pain. A cervical MRI scan revealed a left posterolateral epidural hematoma at the C3–C6 level. The condition of the patient improved after laminectomy and evacuation of the epidural hematoma. The second patient was a 62-year-old man who presented with right hemiparesis and neck pain. A cervical MRI scan revealed a right posterolateral dominant epidural hematoma at the C6-T1 level. The condition of the patient improved after laminectomy and evacuation of the epidural hematoma. The third patient was a 60-year-old woman who presented with left hemiparesis and neck pain. A cervical MRI scan revealed a left posterolateral epidural hematoma at the C2–C4 level. The condition of the patient improved with conservative treatment. The classical clinical presentation of SSEH is acute onset of severe irradiating back pain followed by progression to paralysis, whereas SSEH with hemiparesis is less common. Our cases suggest that acute cervical spinal epidural hematoma should be considered as a differential diagnosis in patients presenting with clinical symptoms of sudden neck pain and radicular pain with progression to hemiparesis.