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Subdural spinal haematoma after spinal anaesthesia in a patient taking aspirin
Journal of Clinical Neuroscience 18 (2011) 1713–1715
Contents lists available at SciVerse ScienceDirect
Journal of Clinical Neuroscience journal homepage: www.elsevier.com/locate/jocn
Case Reports
Subdural spinal haematoma after spinal anaesthesia in a patient taking aspirin Kevin Seow ⇑, Katharine J. Drummond The Department of Neurosurgery, Royal Melbourne Hospital, Grattan Street, Parkville, Victoria 3050, Australia The Department of Surgery, University of Melbourne, Parkville, Victoria, Australia
a r t i c l e
i n f o
Article history: Received 11 October 2010 Accepted 22 March 2011
Keywords: Aspirin Cauda equine Spinal cord compression Subdural spinal haematoma
a b s t r a c t Haematoma in the spinal canal may be catastrophic if the condition is not detected and treated early. In the enclosed spinal canal, even a small space-occupying lesion may be rapidly symptomatic. Clinical presentation ranges from benign back pain to severe neurological deficits, the nature of which depends on the level of compression (cauda equina or spinal cord). Despite surgical decompression and extended rehabilitation, many patients suffer permanent disability. Aspirin use prior to neuraxial block is not generally contraindicated in the literature but we would recommend withholding the anticoagulant, if safe, or considering an alternative form of anaesthesia. Ó 2011 Elsevier Ltd. All rights reserved.
1. Case report
1.1. Surgical management and intra-operative findings
A 63 year-old woman underwent a Zadek’s procedure for bilateral ingrown toenails in a regional hospital. Due to her medical comorbidities, primarily ischaemic heart disease, spinal anaesthesia was used to avoid the risks of general anaesthesia. Prophylactic low-dose aspirin was not withheld prior to spinal anaesthesia. Immediately on introduction of the spinal needle, the patient complained of significant mid-lumbar pain, most intense at the puncture site (‘‘coup de poignard’’). Post-operatively, she was discharged despite non-remitting back pain. One week later, she presented to the Emergency Department with persistent lumbar back pain and was discharged after adequate analgesia. At that time she had no neurological deficit and was afebrile. Over the following week, her pain progressed and radiated into both upper thighs. Her mobility deteriorated and she complained of a 24-hour history of urinary retention requiring in-dwelling catheterisation. On examination, she had lower limb weakness with 4/5 power in her hip flexors bilaterally. Other muscle groups were normal. Deep tendon reflexes were present and symmetrical bilaterally. Her perianal sensation and anal tone were intact. An urgent MRI scan of her lumbosacral spine (Fig. 1) revealed a non-enhancing mass, thought to be an epidural haematoma, thickest at L2/3 causing compression of the cauda equina. The haematoma extended inferiorly to S1 but there was no neural compression below L3. Her blood C-reactive protein, white cell count and platelet count were within the normal range. She was transferred to our unit for urgent L2/3 decompressive laminectomy and evacuation of the haematoma.
Intra-operatively, an L2/3 laminectomy was performed but no epidural haematoma was found. The thecal sac was engorged with a blue discolouration. An intra-operative radiograph was repeated to confirm that surgery was at the correct level. The dura was opened and an acute on chronic thrombus was found in the ventral aspect of the spinal canal, surrounding and adherent to the roots of the cauda equina. The haematoma was evacuated and the nerve roots cleared of as much haematoma as possible. However, adherent inflammatory tissue was not aggressively removed. The dura was closed in a watertight fashion.
⇑ Corresponding author. Tel.: +61 3 93428959; fax: +61 3 93428231. E-mail address: [email protected] (K. Seow).
1.2. Sequelae and follow-up Post-operatively, the patient was clinically stable. She was transferred for rehabilitation and at 6 months had returned to normal baseline function. 2. Discussion 2.1. Spinal haematoma Spinal haematoma was first described at autopsy in 1682 and as a clinical diagnosis in 1867. It is a rare but often catastrophic disorder, often associated with permanent morbidity. Kreppel et al.1 has conducted the largest literature survey so far with a meta-analysis of 613 patients with spinal haematoma reported between 1826 and 1996 (Table 1). A haematoma can affect each of the anatomical layers of the spine. It can occur in the epidural, subdural and subarachnoid compartments2 as well as the intra-medullary tissues. The extradural space is most commonly affected,3 due to the abundance of extra-
1714
Case Reports / Journal of Clinical Neuroscience 18 (2011) 1713–1715
the patients were affected by deficits of homeostasis. This included 19% (n = 20) with known bleeding disorders secondary to leukaemia, haemophillia, thrombocytopaenia, cryoglobulinaemia and polycythaemia, while the remaining 35% (n = 37) were affected by acute or chronic use of anticoagulation agents. The authors also found that spinal puncture had been performed in 47% of patients (n = 50), of whom 33% (n = 35) had coagulation derangement. In the remaining 14% (n = 15) the haematoma resulted from the procedure alone. Most of these iatrogenic cases were associated with technical difficulties or a traumatic tap during the procedure. Sinclair et al.11 reported that a normal coagulation profile and a nontraumatic lumbar puncture does not fully exclude this potential rare complication. Both spinal extradural haematoma (sEDH) and sSDH present with similar clinical symptoms and signs. Differentiation can also be challenging on MRI.12 sEDH is typically characterised by a biconvex-shaped haematoma separated from the intra-dural contents by the hypointense dura on T2-weighted MRI, while sSDH is characterised by a crescent-shaped haematoma located in the deep aspect of the dura, without involvement of the epidural fat.13 Despite the distinct description of these different entities, they are not pathogenomic and the findings may not be confirmed without visual inspection intra-operatively. 2.3. Guidelines for neuraxial block, anticoagulation agents and platelet levels
Fig. 1. (a) Sagittal T2-weighted MRI of the thoracolumbar spine showing the spinal haematoma at L2/3 (arrow); and (b) axial T1-weighted MRI at L2/3 showing the convex lesion suggestive of an ‘‘epidural’’ haematoma (large arrow) and hyperintense signal consistent with epidural fat surrounding the dura (small arrows).
dural veins. Up to 70% of haematomas occur in the thoracolumbar region.3 2.2. Spinal subdural haematoma Spinal subdural haematoma (sSDH) is a rare but welldocumented phenomenon.4,5 It can occur spontaneously with or without concomitant anticoagulation therapies or an inherent defect in haemostasis. It can also be caused by underlying abnormalities, including neoplasms, arteriovenous malformations, arachnoiditis or syringomelia.5–9 sSDH is an established complication of lumbar puncture10 and spinal anaesthesia, with the possibility of permanent disability related to these common procedures. Domenicucci et al.3 reviewed 106 published patients with non-traumatic acute sSDH and found that 54% (n = 57) of
Aspirin is the most commonly used non-steroidal anti-inflammatory drug (NSAID). It is a cyclo-oxygenase-1 inhibitor that irreversibly inhibits platelet function for 7 days to 10 days. During this period, there is a prolonged bleeding time. Several studies have shown relative safety of central neuraxial block (epidural or spinal anaesthesia) with the use of aspirin or other NSAID agents. Horlocker et al.14,15 conducted two prospective trials involving close to 2000 patients and reported no incidence of spinal haematoma. Most authors do not consider the use of aspirin alone as a contraindication to neuraxial block16 but cessation of aspirin 2 days to 3 days prior to neuraxial block is recommended in the setting of concomitant use of other thromboprophylaxis such as heparin. In an obstetric patient population devoid of any risk factors, a platelet count >80 109/L is considered ‘‘safe’’ for placing epidural or spinal anaesthesia, and a platelet count >40 109/L is ‘‘safe’’ for lumbar puncture. With platelet counts lower than these levels, an individual decision should be made based on a risk versus benefit assessment.17 Another author in his retrospective study found that a platelet level of >10 109/L is safe for lumbar puncture.18 2.4. Investigation and treatment of choice MRI is the preferred investigation to elucidate the level and the extent of the haematoma Where MRI is contraindicated, CT myelography can be utilised. The treatment of choice is immediate surgical decompression, particularly in patients with progressive neurological deficits. Non-surgical management is reserved for patients with multiple medical co-morbidities and the absence of neurological deficits. 2.5. Prognosis Spinal haematoma should always be considered as a primary differential diagnosis in patients who complain of back pain after recent neuraxial block or lumbar puncture, regardless of the presence or absence of focal neurological deficits. Repeated presentation with back pain, as occurred in the outpatient department, should be investigated immediately to avoid the onset of neurological deficit. Spontaneous spinal haematoma should also be sus-
Case Reports / Journal of Clinical Neuroscience 18 (2011) 1713–1715 Table 1 Summary of findings of Kreppel et al. of 613 patients with spinal haematoma. After1 Characteristic
Patient details
Age
1–90 years Two peak incidences at 15–20 and 45–75 years
Anatomical site
Epidural, 75.2% Subdural, 4.1% Subarachnoid, 15.7% Intra-medullary, 0.8% Combined/mixed, 2.7% Unknown, 2.7%
Gender M = Male F = Female
Spinal, epidural, subarachnoid haematoma, M:F = 2:1 Subdural haematoma, M:F = 1:1
Segmental site by age
0–44 years: cervico-thoracic > thoraco-lumbar 45–75 years: thoraco-lumbar > cervico-thoracic 76–90 years: cervico-thoracic = thoraco-lumbar
Sagittal localisation
Dorsal and dorsolateral, 75% Ventral and ventrolateral, 9% Circumferential, 16%
Clinical presentation
Complete or incomplete cord/cauda equina lesion, 87.8% Headache, vomiting, papilloedema, nystagmus, seizures, decrease level of consciousness 0.5% Non-specific, 5.9% Unknown, 1.3%
Etiological factors
Idiopathic, 38.2% Coagulation derangement, 28.5% Anti-coagulant,16.9% Bleeding diathesis, 5.6% LP/neuraxial block and anticoagulant, 6.0% LP/neuraxial block, 10.3% Without anticoagulant, 4.3% With anticoagulant, 6.0% Vascular malformation, 9.1% Tumour, 5.7% Trauma with or without fracture, 9.8% Ankylosing spondylitis with or without fracture, 1.1% Other, 2.8%
Treatment
Surgical decompression, 85.8% Conservative, 14.2%
Overall outcome
Complete recovery, 39.6% Incomplete recovery, 48.8% Death, 11.6%
1715
3. Conclusion This rare condition highlights the need for a high index of suspicion after spinal or epidural anaesthesia presenting with pain or neurological signs and symptoms even in the absence of predisposing risk factors. Despite the well-documented low incidence of haematoma after these procedures, even with aspirin use, it would seem prudent to cease all anticoagulants prior to the procedure, if safe to do so. sSDH has a grim prognosis, but early diagnosis and prompt surgical intervention will result in a more favourable outcome. References
pected in patients who complain of progressive spinal cord or nerve root compression symptoms receiving anticoagulant therapy.6 Early recognition determines the management and prognosis, as 50% of patients will be have permanent neurological deficit if the condition is identified more than 12 hours after the onset of symptoms.11 In patients with some post-operative improvement, the prognosis remains guarded as 50% of patients remained disabled and requiring assistance.19 Patients who received immediate surgical intervention and exhibit less severe pre-operative symptoms have a better prognosis for neurological recovery. doi:10.1016/j.jocn.2011.03.016
1. Kreppel D, Antoniadis G, Seeling W. Spinal hematoma: a literature survey with meta-analysis of 613 patients. Neurosurg Rev 2003;26:1–49. 2. Park JH, Shin KM, Hong SJ, et al. Subacute spinal subarachnoid hematoma after spinal anesthesia that causes mild neurologic deterioration. Anesthesiology 2007;107:846–8. 3. Domenicucci M, Ramieri A, Ciappetta P, et al. Nontraumatic acute spinal subdural hematoma – report of five cases and review of the literature. J Neurosurg 1999;91:65–73. 4. Hagen T, Lensch T. Chronic spinal subdural hematoma. Radiologe 2008;48:972–6. 5. Kyriakides AE, Lalam RK, El Masry WS. Acute spontaneous spinal subdural hematoma presenting as paraplegia – a rare case. Spine 2007;32:E619–22. 6. Jimbo H, Asamoto S, Mitsuyama T, et al. Spinal chronic subdural hematoma in association with anticoagulant therapy – a case report and literature review. Spine 2006;31:E184–7. 7. Siddiqi F, Hammod R, Lee D, et al. Spontaneous chronic spinal subdural hematoma associated with spinal arachnoiditis and syringomyelia. J Clin Neurosci 2005;12:949–53. 8. Miller DR, Ray A, Hourihan MD. Spinal subdural haematoma: how relevant is the INR? Spinal Cord 2004;42:477–80. 9. Yamada K, Nakahara T, Yamamato K, et al. Nontraumatic spinal subdural haematoma occurring in a postpartum period. Acta Neurochir 2003;145:151–5. 10. Singh DK, Chauhan M, Gupta V, et al. Spinal subdural hematoma: a rare complication of spinal anesthesia: a case report. Turk Neurosurg 2008;18:324–6. 11. Sinclair AJ, Carroll C, Davies B. Cauda equina syndrome following a lumbar puncture. J Clin Neurosci 2009;16:714–6. 12. Braun P, Kazmi K, Nogués-Meléndez P, et al. MRI findings in spinal subdural and epidural hernatomas. Eur J Radiol 2007;64:119–25. 13. Ohayon L, Gorhan C, Soto-Ares G, et al. Acute spinal epidural and subdural hematomas. J Radiol 2003;84:50–3. 14. Horlocker TT, Wedel DJ, Schroeder DR, et al. Preoperative antiplatelet therapy does not increase the risk of spinal haematoma associated with regional anaesthesia. Anesth Analg 1995;303–9. 15. Horlocker TT, Bajwa ZH, Asraf Z, et al. Risk assessment of hemorrhagic complications associated with nonsteriodal antiinflammatory medications in ambulatory pain clinic patients undergoing epidural steroid injection. Anesth Analg 2002;1691–7. 16. Green L, Machin SJ. Managing anticoagulated patients during neuraxial anaesthesia. Br J Haematol 2010;149:195–208. 17. van Veen JJ, Nokes TJ, Makris M. The risk of spinal haematoma following neuraxial anaesthesia or lumbar puncture in thrombocytopenic individuals. Br J Haematol 2010;148:15–25. 18. Kitanovski L, Trampus-Bakija A, Benedik-Dolnicar M. Prophylactic platelet transfusions before lumbar puncture. Zdrav Vest: Slov Med J 2008;77:I111–5. 19. Thiex R, Thron A, Gilsbach JM, et al. Functional outcome after surgical treatment of spontaneous and nonspontaneous spinal subdural hematomas. J Neurosurg: Spine 2005;3:12–6.
Contents lists available at SciVerse ScienceDirect
Journal of Clinical Neuroscience journal homepage: www.elsevier.com/locate/jocn
Case Reports
Subdural spinal haematoma after spinal anaesthesia in a patient taking aspirin Kevin Seow ⇑, Katharine J. Drummond The Department of Neurosurgery, Royal Melbourne Hospital, Grattan Street, Parkville, Victoria 3050, Australia The Department of Surgery, University of Melbourne, Parkville, Victoria, Australia
a r t i c l e
i n f o
Article history: Received 11 October 2010 Accepted 22 March 2011
Keywords: Aspirin Cauda equine Spinal cord compression Subdural spinal haematoma
a b s t r a c t Haematoma in the spinal canal may be catastrophic if the condition is not detected and treated early. In the enclosed spinal canal, even a small space-occupying lesion may be rapidly symptomatic. Clinical presentation ranges from benign back pain to severe neurological deficits, the nature of which depends on the level of compression (cauda equina or spinal cord). Despite surgical decompression and extended rehabilitation, many patients suffer permanent disability. Aspirin use prior to neuraxial block is not generally contraindicated in the literature but we would recommend withholding the anticoagulant, if safe, or considering an alternative form of anaesthesia. Ó 2011 Elsevier Ltd. All rights reserved.
1. Case report
1.1. Surgical management and intra-operative findings
A 63 year-old woman underwent a Zadek’s procedure for bilateral ingrown toenails in a regional hospital. Due to her medical comorbidities, primarily ischaemic heart disease, spinal anaesthesia was used to avoid the risks of general anaesthesia. Prophylactic low-dose aspirin was not withheld prior to spinal anaesthesia. Immediately on introduction of the spinal needle, the patient complained of significant mid-lumbar pain, most intense at the puncture site (‘‘coup de poignard’’). Post-operatively, she was discharged despite non-remitting back pain. One week later, she presented to the Emergency Department with persistent lumbar back pain and was discharged after adequate analgesia. At that time she had no neurological deficit and was afebrile. Over the following week, her pain progressed and radiated into both upper thighs. Her mobility deteriorated and she complained of a 24-hour history of urinary retention requiring in-dwelling catheterisation. On examination, she had lower limb weakness with 4/5 power in her hip flexors bilaterally. Other muscle groups were normal. Deep tendon reflexes were present and symmetrical bilaterally. Her perianal sensation and anal tone were intact. An urgent MRI scan of her lumbosacral spine (Fig. 1) revealed a non-enhancing mass, thought to be an epidural haematoma, thickest at L2/3 causing compression of the cauda equina. The haematoma extended inferiorly to S1 but there was no neural compression below L3. Her blood C-reactive protein, white cell count and platelet count were within the normal range. She was transferred to our unit for urgent L2/3 decompressive laminectomy and evacuation of the haematoma.
Intra-operatively, an L2/3 laminectomy was performed but no epidural haematoma was found. The thecal sac was engorged with a blue discolouration. An intra-operative radiograph was repeated to confirm that surgery was at the correct level. The dura was opened and an acute on chronic thrombus was found in the ventral aspect of the spinal canal, surrounding and adherent to the roots of the cauda equina. The haematoma was evacuated and the nerve roots cleared of as much haematoma as possible. However, adherent inflammatory tissue was not aggressively removed. The dura was closed in a watertight fashion.
⇑ Corresponding author. Tel.: +61 3 93428959; fax: +61 3 93428231. E-mail address: [email protected] (K. Seow).
1.2. Sequelae and follow-up Post-operatively, the patient was clinically stable. She was transferred for rehabilitation and at 6 months had returned to normal baseline function. 2. Discussion 2.1. Spinal haematoma Spinal haematoma was first described at autopsy in 1682 and as a clinical diagnosis in 1867. It is a rare but often catastrophic disorder, often associated with permanent morbidity. Kreppel et al.1 has conducted the largest literature survey so far with a meta-analysis of 613 patients with spinal haematoma reported between 1826 and 1996 (Table 1). A haematoma can affect each of the anatomical layers of the spine. It can occur in the epidural, subdural and subarachnoid compartments2 as well as the intra-medullary tissues. The extradural space is most commonly affected,3 due to the abundance of extra-
1714
Case Reports / Journal of Clinical Neuroscience 18 (2011) 1713–1715
the patients were affected by deficits of homeostasis. This included 19% (n = 20) with known bleeding disorders secondary to leukaemia, haemophillia, thrombocytopaenia, cryoglobulinaemia and polycythaemia, while the remaining 35% (n = 37) were affected by acute or chronic use of anticoagulation agents. The authors also found that spinal puncture had been performed in 47% of patients (n = 50), of whom 33% (n = 35) had coagulation derangement. In the remaining 14% (n = 15) the haematoma resulted from the procedure alone. Most of these iatrogenic cases were associated with technical difficulties or a traumatic tap during the procedure. Sinclair et al.11 reported that a normal coagulation profile and a nontraumatic lumbar puncture does not fully exclude this potential rare complication. Both spinal extradural haematoma (sEDH) and sSDH present with similar clinical symptoms and signs. Differentiation can also be challenging on MRI.12 sEDH is typically characterised by a biconvex-shaped haematoma separated from the intra-dural contents by the hypointense dura on T2-weighted MRI, while sSDH is characterised by a crescent-shaped haematoma located in the deep aspect of the dura, without involvement of the epidural fat.13 Despite the distinct description of these different entities, they are not pathogenomic and the findings may not be confirmed without visual inspection intra-operatively. 2.3. Guidelines for neuraxial block, anticoagulation agents and platelet levels
Fig. 1. (a) Sagittal T2-weighted MRI of the thoracolumbar spine showing the spinal haematoma at L2/3 (arrow); and (b) axial T1-weighted MRI at L2/3 showing the convex lesion suggestive of an ‘‘epidural’’ haematoma (large arrow) and hyperintense signal consistent with epidural fat surrounding the dura (small arrows).
dural veins. Up to 70% of haematomas occur in the thoracolumbar region.3 2.2. Spinal subdural haematoma Spinal subdural haematoma (sSDH) is a rare but welldocumented phenomenon.4,5 It can occur spontaneously with or without concomitant anticoagulation therapies or an inherent defect in haemostasis. It can also be caused by underlying abnormalities, including neoplasms, arteriovenous malformations, arachnoiditis or syringomelia.5–9 sSDH is an established complication of lumbar puncture10 and spinal anaesthesia, with the possibility of permanent disability related to these common procedures. Domenicucci et al.3 reviewed 106 published patients with non-traumatic acute sSDH and found that 54% (n = 57) of
Aspirin is the most commonly used non-steroidal anti-inflammatory drug (NSAID). It is a cyclo-oxygenase-1 inhibitor that irreversibly inhibits platelet function for 7 days to 10 days. During this period, there is a prolonged bleeding time. Several studies have shown relative safety of central neuraxial block (epidural or spinal anaesthesia) with the use of aspirin or other NSAID agents. Horlocker et al.14,15 conducted two prospective trials involving close to 2000 patients and reported no incidence of spinal haematoma. Most authors do not consider the use of aspirin alone as a contraindication to neuraxial block16 but cessation of aspirin 2 days to 3 days prior to neuraxial block is recommended in the setting of concomitant use of other thromboprophylaxis such as heparin. In an obstetric patient population devoid of any risk factors, a platelet count >80 109/L is considered ‘‘safe’’ for placing epidural or spinal anaesthesia, and a platelet count >40 109/L is ‘‘safe’’ for lumbar puncture. With platelet counts lower than these levels, an individual decision should be made based on a risk versus benefit assessment.17 Another author in his retrospective study found that a platelet level of >10 109/L is safe for lumbar puncture.18 2.4. Investigation and treatment of choice MRI is the preferred investigation to elucidate the level and the extent of the haematoma Where MRI is contraindicated, CT myelography can be utilised. The treatment of choice is immediate surgical decompression, particularly in patients with progressive neurological deficits. Non-surgical management is reserved for patients with multiple medical co-morbidities and the absence of neurological deficits. 2.5. Prognosis Spinal haematoma should always be considered as a primary differential diagnosis in patients who complain of back pain after recent neuraxial block or lumbar puncture, regardless of the presence or absence of focal neurological deficits. Repeated presentation with back pain, as occurred in the outpatient department, should be investigated immediately to avoid the onset of neurological deficit. Spontaneous spinal haematoma should also be sus-
Case Reports / Journal of Clinical Neuroscience 18 (2011) 1713–1715 Table 1 Summary of findings of Kreppel et al. of 613 patients with spinal haematoma. After1 Characteristic
Patient details
Age
1–90 years Two peak incidences at 15–20 and 45–75 years
Anatomical site
Epidural, 75.2% Subdural, 4.1% Subarachnoid, 15.7% Intra-medullary, 0.8% Combined/mixed, 2.7% Unknown, 2.7%
Gender M = Male F = Female
Spinal, epidural, subarachnoid haematoma, M:F = 2:1 Subdural haematoma, M:F = 1:1
Segmental site by age
0–44 years: cervico-thoracic > thoraco-lumbar 45–75 years: thoraco-lumbar > cervico-thoracic 76–90 years: cervico-thoracic = thoraco-lumbar
Sagittal localisation
Dorsal and dorsolateral, 75% Ventral and ventrolateral, 9% Circumferential, 16%
Clinical presentation
Complete or incomplete cord/cauda equina lesion, 87.8% Headache, vomiting, papilloedema, nystagmus, seizures, decrease level of consciousness 0.5% Non-specific, 5.9% Unknown, 1.3%
Etiological factors
Idiopathic, 38.2% Coagulation derangement, 28.5% Anti-coagulant,16.9% Bleeding diathesis, 5.6% LP/neuraxial block and anticoagulant, 6.0% LP/neuraxial block, 10.3% Without anticoagulant, 4.3% With anticoagulant, 6.0% Vascular malformation, 9.1% Tumour, 5.7% Trauma with or without fracture, 9.8% Ankylosing spondylitis with or without fracture, 1.1% Other, 2.8%
Treatment
Surgical decompression, 85.8% Conservative, 14.2%
Overall outcome
Complete recovery, 39.6% Incomplete recovery, 48.8% Death, 11.6%
1715
3. Conclusion This rare condition highlights the need for a high index of suspicion after spinal or epidural anaesthesia presenting with pain or neurological signs and symptoms even in the absence of predisposing risk factors. Despite the well-documented low incidence of haematoma after these procedures, even with aspirin use, it would seem prudent to cease all anticoagulants prior to the procedure, if safe to do so. sSDH has a grim prognosis, but early diagnosis and prompt surgical intervention will result in a more favourable outcome. References
pected in patients who complain of progressive spinal cord or nerve root compression symptoms receiving anticoagulant therapy.6 Early recognition determines the management and prognosis, as 50% of patients will be have permanent neurological deficit if the condition is identified more than 12 hours after the onset of symptoms.11 In patients with some post-operative improvement, the prognosis remains guarded as 50% of patients remained disabled and requiring assistance.19 Patients who received immediate surgical intervention and exhibit less severe pre-operative symptoms have a better prognosis for neurological recovery. doi:10.1016/j.jocn.2011.03.016
1. Kreppel D, Antoniadis G, Seeling W. Spinal hematoma: a literature survey with meta-analysis of 613 patients. Neurosurg Rev 2003;26:1–49. 2. Park JH, Shin KM, Hong SJ, et al. Subacute spinal subarachnoid hematoma after spinal anesthesia that causes mild neurologic deterioration. Anesthesiology 2007;107:846–8. 3. Domenicucci M, Ramieri A, Ciappetta P, et al. Nontraumatic acute spinal subdural hematoma – report of five cases and review of the literature. J Neurosurg 1999;91:65–73. 4. Hagen T, Lensch T. Chronic spinal subdural hematoma. Radiologe 2008;48:972–6. 5. Kyriakides AE, Lalam RK, El Masry WS. Acute spontaneous spinal subdural hematoma presenting as paraplegia – a rare case. Spine 2007;32:E619–22. 6. Jimbo H, Asamoto S, Mitsuyama T, et al. Spinal chronic subdural hematoma in association with anticoagulant therapy – a case report and literature review. Spine 2006;31:E184–7. 7. Siddiqi F, Hammod R, Lee D, et al. Spontaneous chronic spinal subdural hematoma associated with spinal arachnoiditis and syringomyelia. J Clin Neurosci 2005;12:949–53. 8. Miller DR, Ray A, Hourihan MD. Spinal subdural haematoma: how relevant is the INR? Spinal Cord 2004;42:477–80. 9. Yamada K, Nakahara T, Yamamato K, et al. Nontraumatic spinal subdural haematoma occurring in a postpartum period. Acta Neurochir 2003;145:151–5. 10. Singh DK, Chauhan M, Gupta V, et al. Spinal subdural hematoma: a rare complication of spinal anesthesia: a case report. Turk Neurosurg 2008;18:324–6. 11. Sinclair AJ, Carroll C, Davies B. Cauda equina syndrome following a lumbar puncture. J Clin Neurosci 2009;16:714–6. 12. Braun P, Kazmi K, Nogués-Meléndez P, et al. MRI findings in spinal subdural and epidural hernatomas. Eur J Radiol 2007;64:119–25. 13. Ohayon L, Gorhan C, Soto-Ares G, et al. Acute spinal epidural and subdural hematomas. J Radiol 2003;84:50–3. 14. Horlocker TT, Wedel DJ, Schroeder DR, et al. Preoperative antiplatelet therapy does not increase the risk of spinal haematoma associated with regional anaesthesia. Anesth Analg 1995;303–9. 15. Horlocker TT, Bajwa ZH, Asraf Z, et al. Risk assessment of hemorrhagic complications associated with nonsteriodal antiinflammatory medications in ambulatory pain clinic patients undergoing epidural steroid injection. Anesth Analg 2002;1691–7. 16. Green L, Machin SJ. Managing anticoagulated patients during neuraxial anaesthesia. Br J Haematol 2010;149:195–208. 17. van Veen JJ, Nokes TJ, Makris M. The risk of spinal haematoma following neuraxial anaesthesia or lumbar puncture in thrombocytopenic individuals. Br J Haematol 2010;148:15–25. 18. Kitanovski L, Trampus-Bakija A, Benedik-Dolnicar M. Prophylactic platelet transfusions before lumbar puncture. Zdrav Vest: Slov Med J 2008;77:I111–5. 19. Thiex R, Thron A, Gilsbach JM, et al. Functional outcome after surgical treatment of spontaneous and nonspontaneous spinal subdural hematomas. J Neurosurg: Spine 2005;3:12–6.