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Postoperative Hematoma in Cranial and Spinal Surgery
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Postoperative Hematoma in Cranial and Spinal Surgery ANIL NANDA, AMEY R. SAVARDEKAR
HIGHLIGHTS • The cranial perspective • Postoperative hemorrhage is one of the most serious complications of any cranial neurosurgical procedure. • The incidence figures for clinically significant postoperative hemorrhage for cranial surgery ranges from 0.8% to 6.9%. • Hemostatic disturbances including coagulopathy and thrombocytopenia, as well as administration of antiplatelet agents, have been identified as general risk factors for postoperative hematomas after neurosurgical procedures. • Many of the best recommendation practices for preventing, detecting, and treating postoperative hemorrhage seem intuitive and are likely to be in practice in most neurosurgery units; however, dealing with this iatrogenic disaster just comes down to “doing the simple things right, each and every time.” • The spinal perspective • Symptomatic postoperative spinal epidural hematoma is a rare, yet well-recognized, complication of spinal surgery with the potential for leaving patients with devastating consequences. • The reported incidence of symptomatic postoperative spinal epidural hematoma in the literature varies significantly from 0.1% up to 1%. • Most clinically significant postoperative spinal epidural hematomas occur in the first few hours after surgery, highlighting the importance of close neurologic monitoring of patients during this period. • It usually requires emergent surgical evacuation, and early intervention is likely to result in better neurologic recovery. • Larger studies are needed to accurately identify those at high risk of developing spinal epidural hematoma after spinal surgery.
“The practice of neurosurgery, inherently, is more sensitive to any deficit in hemostasis than many of the other surgical disciplines.” MERRIMAN ET AL. (1970)
Introduction Postoperative hemorrhage (POH) can develop after any neurosurgical operation and tends to have a devastating effect on the outcome, if not detected at an early stage. Thus avoidance of such a complication is of vital interest. Merriman et al. accurately noted “the practice
of neurosurgery, inherently, is more sensitive to any deficit in hemostasis than many of the other surgical disciplines.”1 This puts the impetus squarely on the operating neurosurgeon to prevent this postoperative complication and, in the event of its occurrence, to detect and treat it early before the patient develops a lasting neurologic deficit. Due to the variation in the presentation, detection, and management of this complication in cranial vis-à-vis spinal surgery, we have dealt with these in two separate sections.
The Cranial Perspective POH is one of the most serious complications of any cranial neurosurgical procedure. A number of studies have demonstrated the significant morbidity and mortality associated with intracranial bleeding after neurosurgery.2 The rates of POH after intracranial procedures reported in the literature vary greatly, ranging from 0.8% to 50.0%.3 However, meaningful comparison is difficult due to the variance in the definition of POH. It is generally defined as bleeding at the operative site after surgery; however, it may be argued that in most operative beds, some residual blood is to be expected. Also, it is clinico-radiologically difficult to acutely differentiate between expected residual blood and small de novo hemorrhages that are benign.4 Incidence figures thus vary depending on definition, with rates of 0.8% to 6.9% reported for postoperative clinical deterioration and rates of 10.8% to 50.0% based on routine radiologic monitoring.3 Postoperative clinical deterioration is the most consistent sign directing clinicians to suspect significant intracranial hematoma.5 Hence, as per existing literature, the best definition for a postoperative intracranial hemorrhage is a hematoma, which is clinically significant and requires surgical evacuation.3,4
Location of Postoperative Hemorrhage POH after a cranial surgery can occur at any of the following locations: epidural, subdural, intraparenchymal, remote, or mixed. Many studies have found that the majority of postoperative hematomas were epidural or intraparenchymal.2 Kalfas and Little analyzed a series of 4992 intracranial procedures performed over an 11-year period for the occurrence of POH.5 Forty patients (0.8%) experienced POH, out of which 24 (60%) were intracerebral, 11 (28%) were epidural, 3 (7.5%) were subdural, and 2 (5%) were intrasellar. POH in 33 patients occurred at the operative site, and in 7 it occurred remote from the operative site. Palmer et al., in a review of 6668 operations performed over 5 years, reported 71 27
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surgically evacuated POH, accounting for an incidence of 1.1%.6 POHs were intraparenchymal in 43% of cases, subdural in 5%, extradural in 33%, mixed in 8%, and confined to the superficial wound in 11%. In a study by Gerlach et al., 21 out of 296 patients operated for intracranial meningiomas developed a POH and needed resurgery.7 Out of those 21, 9 patients had extradural hematoma (EDH), 3 patients had intraparenchymal hematoma (IPH), and the remaining 9 patients had mixed [EDH/subdural hematoma(SDH)/ IPH] hematomas. In 2305 cranial neurosurgical procedures reviewed by Taylor et al., 50 (2.2%) developed a hematoma.8 The hematomas were extradural in 26 patients (52%), intracerebral in 22 (44%) patients, and subdural in two (4%) patients. Remote intracerebral hemorrhage is a rare complication of craniotomy with significant morbidity and mortality.3,9 Brisman et al. reviewed 37 cases of remote POH occurring after cranial neurosurgery and concluded that such hemorrhages likely develop at or soon after surgery, tend to occur preferentially in certain locations, and can be related to the craniotomy site, operative positioning, and nonspecific mechanical factors.9 They are not related to hypertension, coagulopathy, cerebrospinal fluid drainage, or underlying pathologic abnormalities.
Analysis of Causative Factors A postoperative hematoma after elective surgery can have a devastating effect on the patient’s outcome. However, in most of the patients with POH, no obvious cause for the hematoma can be found; it is related neither to the surgical technique nor to hemostatic parameters. Various predisposing risk factors have been analyzed: Hypertension was generally found to be significant in most studies, whereas diabetes mellitus, cerebral amyloid angiopathy, and atherosclerosis were generally not significant.3,5 Basali et al. noted that patients with postoperative intracranial hemorrhage had a significantly greater rate of intraoperative and postoperative/prehemorrhage hypertension.10 Intraoperative hypertension occurs during brain manipulation, head pin application, use of epinephrine containing anesthetics, periosteal dissection, and emergence. Basali et al. also found a significantly high odds ratio for intracranial hemorrhage when patients had blood pressure <160/90 intraoperatively but then had elevated blood pressure postoperatively.10 This suggests that some vessels may not have been adequately tested intraoperatively for the possibility of leaking when blood pressure rises.10 Age is a significant risk factor for hematoma development— sixfold more likely at age over 70 and 12-fold over 75.7,11 It remains speculative why the risk of bleeding increases with age. It can be speculated that POH in the elderly is attributed to changes in the blood vessels themselves and to the function of platelets. It was found that elderly patients have more thrombin activation/ generation and fibrinolytic activity before surgery than younger patients.7 Other risk factors include antiplatelet use, including aspirin and nonsteroidal antiinflammatory drugs, preoperative mannitol administration, excessive alcohol use, coagulopathies, disseminated intravascular coagulation, thrombocytopenia, acute decreases in platelet counts postoperatively, excessive intraoperative blood loss, poor response to preoperative platelet transfusions, factor XIII deficiencies, and decreased fibrinogen levels.1–4,7 One might expect that surgeons with greater levels of experience should encounter fewer postoperative hematomas. However, in the study by Taylor et al., there was no correlation between the rank of the surgeon and the occurrence of postoperative hematoma, with 27 hematomas (54%) occurring after operations by consultants and 23 (46%) after operations by registrars or senior registrars.8
Kim et al. conclude that large intraoperative blood loss and wide craniotomy area are risk factors for postoperative EDH after intracranial surgery.12 However, this study had significant limitations because it did not examine the role of established risk factors for POH. In another series of patients, who underwent surgery to remove brain tumors, the highest rate of postoperative hematomas was found after meningioma surgery.7 POH remains a major cause of poor outcome after meningioma surgery.
Timing of Occurrence of Postoperative Hemorrhage and Overall Outcome Gerlach et al. found that the majority of their hematomas were discovered within 3 days of the initial operation.7 Kalfas and Little found that 35% of their ICH cases were discovered within 12 hours.5 Taylor et al., in their review of 2305 patients in which 50 developed postoperative hematomas, noted that 44 out of the 50 developed within 6 hours.8 What has emerged through the literature review is that there are two distinct time periods in which neurologic deterioration secondary to a hematoma occurs, the first being within 6 hours of surgery and the second being 24 hours or more from the time of surgery. The first group likely represents continued active bleeding at the operative site, and the second group represents patients in whom active bleeding is likely to have come to a halt; their clinical deterioration may represent secondary swelling and edema formation around the hematoma. Desai et al., in their review of 3109 cranial operations, noted that when the initial operation was for evacuation of intraparenchymal hematoma, the return to the operating room for evacuation of a postoperative hematoma occurred sooner than for any other type of operation.2 Generally, outcome is poor with a range of mortality from 13% to 41% depending on the type of initial operation (tumor vs traumatic ICH, etc.). Good recovery, defined as Glasgow Outcome Scale (GOS) 4 or 5, has been reported in the range of 39% to 71% of the cases in which POH developed.4−7
Strategies—Preventive and Treatment Close clinical and neurologic observations in the immediate postoperative period are the usual means of POH detection.3 Failure to adequately awaken from general anesthesia or deterioration of observation parameters would prompt for an urgent scan to check for and treat POH. Thus, our recommendations for clinical practice based on the literature reviewed would include: 1. Preoperative: Cease any antiplatelet and anticoagulant therapy for an adequate period; stop alcohol consumption; ensure platelet count, function, and coagulation parameters are normal; consider factor XIII screening; and optimize medical management of preexisting conditions, particularly hypertension. 2. Intraoperative: Avoid hypertension and excessive blood loss; replace blood losses promptly and sufficiently; aim for gross total resection of tumor wherever possible; meticulous technique and hemostasis including dural tenting, appropriate use of electrocoagulation and topical hemostats; Valsalva maneuver at the end of surgery; and a slow, gentle wean from general anesthesia. 3. Postoperative: Avoid hypertension; replace blood losses adequately; avoid upright patient positioning in the initial phase; close clinical monitoring in the first 6 h postsurgery; consider ICP monitoring or early postoperative imaging. ICP monitoring may be useful if there have been significant problems with hemostasis during surgery, if the lesion has been very vascular,
CHAPTER 7 Postoperative Hematoma in Cranial and Spinal Surgery
if blood loss has been great during surgery, or if the patient needs to remain sedated and/or ventilated after surgery.
The Spinal Perspective Symptomatic postoperative spinal epidural hematoma (SEH) is a rare, yet well-recognized, complication of spinal surgery with potentially devastating consequences.13 Some common complications, such as an incidental durotomy, have little long-term clinical impact; conversely, some rare complications, such as a clinically significant SEH, can lead to permanent neurologic deficits.14 Most patients after spinal surgery demonstrate a varying degree of epidural hematoma on imaging; however, most remain asymptomatic.13 It is therefore impractical and unnecessary to perform a postoperative MRI scan on all patients.13,14 However, prompt attention should be paid to patients who develop either new or deteriorating neurologic signs and symptoms postoperatively.15 In this section, we discuss the incidence, associated risk factors, diagnosis, and management strategies for this rare but important complication of spinal surgery.
Incidence of Postoperative Symptomatic Spinal Epidural Hematoma The actual incidence of clinically silent epidural hematoma is reported to be much higher than that found for symptomatic hematomas. Postoperative SEH is a common radiologic finding identified in 33% to 100% of surgical cases by computed tomography (CT) scan or magnetic resonance imaging (MRI).16 For example, in patients undergoing lumbar surgery, Sokolowski et al. identified a 58% incidence of asymptomatic postoperative epidural hematoma (diagnosed by MRI) compressing the thecal sac beyond its preoperative state at one or more levels.17 The majority of radiologically diagnosed SEHs are clinically silent. As per literature review, most authors define a postoperative SEH as one that is clinically symptomatic rather than one that is asymptomatic and diagnosed by radiology alone. Kao et al. reviewed over 15,500 lumbar spine surgeries and identified 25 patients with a symptomatic postoperative SEH for an incidence of 0.16%.18 Awad et al. reviewed almost 15,000 consecutive spine cases at a single institution and identified 32 cases (0.2%) of symptomatic postoperative SEH.19 In a study by Kou et al., out of approximately 12,000 spinal procedures performed over a 10-year period, 12 patients (0.1%) were identified who developed a new postoperative neurologic deficit that was surgically confirmed to be caused by a postoperative SEH.20 All cases involved lumbar laminectomies. Aono et al. reported on 6356 spinal surgeries and identified 26 (0.41%) patients with symptomatic postoperative SEH.21 The authors also identified the incidence by procedure. Zero hematomas were seen in 1568 lumbar discectomies; eight were identified in 1614 patients undergoing a lumbar laminectomy (0.5%), and eight were identified in 1191 patients undergoing a posterior lumbar interbody fusion (0.67%). As per the abovementioned articles and a detailed review of literature, the risk of a clinically significant postoperative SEH appears to be low, the range being between 0% and 1%.13,15
Risk Factors for Postoperative Spinal Epidural Hematoma The ensuing morbidity of postoperative SEH is substantial, and therefore it is a feared complication of spinal surgery.21 Identification of potentially modifiable risk factors or preventive measures is of
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value to help decrease the risk of hematoma development in this patient population.16 The rarity of this complication makes it difficult to study or draw conclusions on regarding potential predisposing risk factors. Although multiple large studies have been performed attempting to identify risk factors for this complication, there is still significant debate about the effect of subfascial drains, postoperative anticoagulation, and antiplatelet medication on the incidence of postoperative hematoma. Although there is no evidence that use of prophylactic doses of anticoagulation increases the risk of a symptomatic postoperative epidural hematoma, there is insufficient data available in the literature to define the safety profile of postoperative prophylactic anticoagulation. Kao et al. performed a case-control analysis to identify risk factors.18 Despite looking at over 20 possible risk factors including age, the use of anticoagulants, platelet count, and blood loss, the only significant risk factors for the development of a symptomatic SEH identified by the authors were an elevated preoperative diastolic blood pressure, the intraoperative use of Gelfoam for dura coverage, and high postoperative drain output. Awad et al. found the following risk factors associated with postoperative SEH: Preoperative risk factors included the use of nonsteroidal antiinflammatories, Rhpositive blood, and age above 60 years; intraoperative risk factors included surgeries involving >5 levels, significant blood loss of >1 L, and a hemoglobin of <10 g/dL; postoperative risk factors included Coumadin use only if the international normalized ratio (INR) was >2.0 in the first 48 hours.19 They also found that well-controlled anticoagulation and the use of drains were not associated with an increased risk of postoperative SEH. Kou et al. conclude that patients who require multilevel lumbar procedures and/or have a preoperative coagulopathy are at a significantly higher risk for developing a postoperative epidural hematoma. They suggest that extra precautions for meticulous hemostasis during the surgical procedure should be considered in such patients and that postoperative neurologic examinations be done routinely for them.20 Amiri et al., in their review of 4568 open spinal operations, found alcohol consumption greater than 10 units a week, multilevel procedure, and previous spinal surgery as risk factors for developing SEH.13 Studies specifically evaluating whether the presence of a postoperative subfascial drain affected the risk of symptomatic epidural hematoma have not found a significant protective effect from the use of a drain.13,19,20 Similarly, a metaanalysis looking at the effect of drain use after all orthopedic procedures found that there was no decrease in the rate of a postoperative hematoma with the use of a closed suction surgical drain.22 However, the use of a drain did lead to an increase in the need for blood transfusions. Despite the lack of evidence that subfascial drains decrease the risk of a symptomatic postoperative epidural hematoma, drains are still commonly used in lumbar spine surgery because they have been shown to decrease the risk of an asymptomatic postoperative epidural hematoma.23,24 In a prospective study in which a lumbar spine MRI was obtained on postoperative day 1 in 50 patients who underwent lumbar spine surgery, Mirzai et al. reported that the use of a drain significantly decreased the incidence of an asymptomatic epidural hematoma from 89% to 36%.24 Importantly, none of the patients in either of these studies had evidence of neurologic deficit related to the epidural hematomas.
Diagnosis and Management of Symptomatic Postoperative Spinal Epidural Hematoma Once SEH has occurred, it is important to act rapidly to minimize any lasting disability. Delay in surgical evacuation has previously
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resulted in a successful litigation case.13 Almost all patients who develop a symptomatic postoperative epidural hematoma have some evidence of neurologic compromise.14 The symptoms of SEH usually occur within 24 hours after the initial surgery.18,21 Kao et al. reported that 80% of patients with a lumbar epidural hematoma presented with progressive loss of postoperative muscle strength, 76% presented with some amount of saddle anesthesia, and 56% presented with a sudden severe increase in pain.18 When any of these symptoms are present, the patient should undergo an emergent MRI to evaluate for a possible epidural hematoma. It is preferred to obtain an MRI on all patients with new neurologic findings postoperatively to ensure that the diagnosis of a postoperative SEH is not missed or delayed. Most authors agree that emergent surgical evacuation should be performed as soon as possible when neurologic deterioration is detected and postoperative SEH is suspected.14,15,25 Delamarter et al. have demonstrated, in a model of dogs, that recovery from spinal cord compression is inversely associated with duration of compression, and that demyelination after compression occurs in direct proportion to the duration of compression.26 Kebaish and Awad concluded that if patients undergo evacuation operation within 6 hours of symptom onset of postoperative deficit, the neurologic outcomes are usually better.27 In a study of 30 cases of epidural hematoma with neurologic deficit due to various causes such as spinal surgery and anticoagulation medications, Lawton et al. revealed that the rapidity of taking patients to re-operation correlated with better neurological outcomes.25 Hence, symptomatic postoperative SEH should be suspected in any patient with a new-onset neurologic deterioration in the postoperative period; the patient should be diagnosed with an MRI or CT (if urgent neuroimaging is possible), and an emergent decompression surgery should be performed as early as possible.
Conclusion “A stitch in time saves nine.” POH in neurosurgery is a harbinger of poor neurologic outcome and hence should be given due importance. It is imperative to check hemodynamic and coagulation factors before taking up a patient for any neurosurgical procedure. However, the truth of the matter is that even after doing everything right both preoperatively and intraoperatively, POH can occur even in the absence of any risk factors. The neurosurgeon always has to be vigilant toward this dreaded complication. An examination/imaging study in time saves the patient valuable neurons and significantly improves the overall outcome.
References 1. Merriman E, Bell W, Long DM. Surgical postoperative bleeding associated with aspirin ingestion. Report of two cases. J Neurosurg. 1979;50(5):682–684. 2. Desai VR, Grossman R, Sparrow H. Incidence of intracranial hemorrhage after a cranial operation. Cureus. 2016;8:e616. 3. Seifman MA, Lewis PM, Rosenfeld JV, Hwang PY. Postoperative intracranial haemorrhage: a review. Neurosurg Rev. 2011;34:393–407. 4. Bullock R, Hanemann CO, Murray L, Teasdale GM. Recurrent hematomas following craniotomy for traumatic intracranial mass. J Neurosurg. 1990;72:9–14. 5. Kalfas IH, Little JR. Postoperative hemorrhage: a survey of 4992 intracranial procedures. Neurosurgery. 1988;23:343–347. 6. Palmer JD, Sparrow OC, Iannotti F. Postoperative hematoma: a 5-year survey and identification of avoidable risk factors. Neurosurgery. 1994;35:1061–1064, discussion 1064–1065.
7. Gerlach R, Raabe A, Scharrer I, Meixensberger J, Seifert V. Postoperative hematoma after surgery for intracranial meningiomas: causes, avoidable risk factors and clinical outcome. Neurol Res. 2004;26:61–66. 8. Taylor WA, Thomas NW, Wellings JA, Bell BA. Timing of postoperative intracranial hematoma development and implications for the best use of neurosurgical intensive care. J Neurosurg. 1995;82:48–50. 9. Brisman MH, Bederson JB, Sen CN, Germano IM, Moore F, Post KD. Intracerebral hemorrhage occurring remote from the craniotomy site. Neurosurgery. 1996;39:1114–1121, discussion 1121-1112. 10. Basali A, Mascha EJ, Kalfas I, Schubert A. Relation between perioperative hypertension and intracranial hemorrhage after craniotomy. Anesthesiology. 2000;93:48–54. 11. Gerlach R, Tolle F, Raabe A, Zimmermann M, Siegemund A, Seifert V. Increased risk for postoperative hemorrhage after intracranial surgery in patients with decreased factor XIII activity: implications of a prospective study. Stroke. 2002;33:1618–1623. 12. Kim SH, Lee JH, Joo W, et al. Analysis of the risk factors for development of post-operative extradural hematoma after intracranial surgery. Br J Neurosurg. 2015;29:243–248. 13. Amiri AR, Fouyas IP, Cro S, Casey AT. Postoperative spinal epidural hematoma (SEH): incidence, risk factors, onset, and management. Spine J. 2013;13:134–140. 14. Schroeder GD, Kurd MF, Kepler CK, Arnold PM, Vaccaro AR. Postoperative epidural hematomas in the lumbar spine. J Spinal Disord Tech. 2015;28:313–318. 15. Glotzbecker MP, Bono CM, Wood KB, Harris MB. Postoperative spinal epidural hematoma: a systematic review. Spine. 2010;35:E413– E420. 16. Goldstein CL, Bains I, Hurlbert RJ. Symptomatic spinal epidural hematoma after posterior cervical surgery: incidence and risk factors. Spine J. 2015;15:1179–1187. 17. Sokolowski MJ, Garvey TA, Perl J 2nd, et al. Prospective study of postoperative lumbar epidural hematoma: incidence and risk factors. Spine. 2008;33:108–113. 18. Kao FC, Tsai TT, Chen LH, et al. Symptomatic epidural hematoma after lumbar decompression surgery. Eur Spine J. 2015;24:348–357. 19. Awad JN, Kebaish KM, Donigan J, Cohen DB, Kostuik JP. Analysis of the risk factors for the development of post-operative spinal epidural haematoma. J Bone Joint Surg Br. 2005;87:1248–1252. 20. Kou J, Fischgrund J, Biddinger A, Herkowitz H. Risk factors for spinal epidural hematoma after spinal surgery. Spine. 2002;27:1670– 1673. 21. Aono H, Ohwada T, Hosono N, et al. Incidence of postoperative symptomatic epidural hematoma in spinal decompression surgery. J Neurosurg Spine. 2011;15:202–205. 22. Parker MJ, Livingstone V, Clifton R, McKee A. Closed suction surgical wound drainage after orthopaedic surgery. Cochrane Database Syst Rev. 2007;(3):CD001825. 23. Leonardi MA, Zanetti M, Saupe N, Min K. Early postoperative MRI in detecting hematoma and dural compression after lumbar spinal decompression: prospective study of asymptomatic patients in comparison to patients requiring surgical revision. Eur Spine J. 2010;19:2216–2222. 24. Mirzai H, Eminoglu M, Orguc S. Are drains useful for lumbar disc surgery? A prospective, randomized clinical study. J Spinal Disord Tech. 2006;19:171–177. 25. Lawton MT, Porter RW, Heiserman JE, Jacobowitz R, Sonntag VK, Dickman CA. Surgical management of spinal epidural hematoma: relationship between surgical timing and neurological outcome. J Neurosurg. 1995;83:1–7. 26. Delamarter RB, Sherman J, Carr JB. Pathophysiology of spinal cord injury. Recovery after immediate and delayed decompression. J Bone Joint Surg Am. 1995;77:1042–1049. 27. Kebaish KM, Awad JN. Spinal epidural hematoma causing acute cauda equina syndrome. Neurosurg Focus. 2004;16:e1.
Postoperative Hematoma in Cranial and Spinal Surgery ANIL NANDA, AMEY R. SAVARDEKAR
HIGHLIGHTS • The cranial perspective • Postoperative hemorrhage is one of the most serious complications of any cranial neurosurgical procedure. • The incidence figures for clinically significant postoperative hemorrhage for cranial surgery ranges from 0.8% to 6.9%. • Hemostatic disturbances including coagulopathy and thrombocytopenia, as well as administration of antiplatelet agents, have been identified as general risk factors for postoperative hematomas after neurosurgical procedures. • Many of the best recommendation practices for preventing, detecting, and treating postoperative hemorrhage seem intuitive and are likely to be in practice in most neurosurgery units; however, dealing with this iatrogenic disaster just comes down to “doing the simple things right, each and every time.” • The spinal perspective • Symptomatic postoperative spinal epidural hematoma is a rare, yet well-recognized, complication of spinal surgery with the potential for leaving patients with devastating consequences. • The reported incidence of symptomatic postoperative spinal epidural hematoma in the literature varies significantly from 0.1% up to 1%. • Most clinically significant postoperative spinal epidural hematomas occur in the first few hours after surgery, highlighting the importance of close neurologic monitoring of patients during this period. • It usually requires emergent surgical evacuation, and early intervention is likely to result in better neurologic recovery. • Larger studies are needed to accurately identify those at high risk of developing spinal epidural hematoma after spinal surgery.
“The practice of neurosurgery, inherently, is more sensitive to any deficit in hemostasis than many of the other surgical disciplines.” MERRIMAN ET AL. (1970)
Introduction Postoperative hemorrhage (POH) can develop after any neurosurgical operation and tends to have a devastating effect on the outcome, if not detected at an early stage. Thus avoidance of such a complication is of vital interest. Merriman et al. accurately noted “the practice
of neurosurgery, inherently, is more sensitive to any deficit in hemostasis than many of the other surgical disciplines.”1 This puts the impetus squarely on the operating neurosurgeon to prevent this postoperative complication and, in the event of its occurrence, to detect and treat it early before the patient develops a lasting neurologic deficit. Due to the variation in the presentation, detection, and management of this complication in cranial vis-à-vis spinal surgery, we have dealt with these in two separate sections.
The Cranial Perspective POH is one of the most serious complications of any cranial neurosurgical procedure. A number of studies have demonstrated the significant morbidity and mortality associated with intracranial bleeding after neurosurgery.2 The rates of POH after intracranial procedures reported in the literature vary greatly, ranging from 0.8% to 50.0%.3 However, meaningful comparison is difficult due to the variance in the definition of POH. It is generally defined as bleeding at the operative site after surgery; however, it may be argued that in most operative beds, some residual blood is to be expected. Also, it is clinico-radiologically difficult to acutely differentiate between expected residual blood and small de novo hemorrhages that are benign.4 Incidence figures thus vary depending on definition, with rates of 0.8% to 6.9% reported for postoperative clinical deterioration and rates of 10.8% to 50.0% based on routine radiologic monitoring.3 Postoperative clinical deterioration is the most consistent sign directing clinicians to suspect significant intracranial hematoma.5 Hence, as per existing literature, the best definition for a postoperative intracranial hemorrhage is a hematoma, which is clinically significant and requires surgical evacuation.3,4
Location of Postoperative Hemorrhage POH after a cranial surgery can occur at any of the following locations: epidural, subdural, intraparenchymal, remote, or mixed. Many studies have found that the majority of postoperative hematomas were epidural or intraparenchymal.2 Kalfas and Little analyzed a series of 4992 intracranial procedures performed over an 11-year period for the occurrence of POH.5 Forty patients (0.8%) experienced POH, out of which 24 (60%) were intracerebral, 11 (28%) were epidural, 3 (7.5%) were subdural, and 2 (5%) were intrasellar. POH in 33 patients occurred at the operative site, and in 7 it occurred remote from the operative site. Palmer et al., in a review of 6668 operations performed over 5 years, reported 71 27
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surgically evacuated POH, accounting for an incidence of 1.1%.6 POHs were intraparenchymal in 43% of cases, subdural in 5%, extradural in 33%, mixed in 8%, and confined to the superficial wound in 11%. In a study by Gerlach et al., 21 out of 296 patients operated for intracranial meningiomas developed a POH and needed resurgery.7 Out of those 21, 9 patients had extradural hematoma (EDH), 3 patients had intraparenchymal hematoma (IPH), and the remaining 9 patients had mixed [EDH/subdural hematoma(SDH)/ IPH] hematomas. In 2305 cranial neurosurgical procedures reviewed by Taylor et al., 50 (2.2%) developed a hematoma.8 The hematomas were extradural in 26 patients (52%), intracerebral in 22 (44%) patients, and subdural in two (4%) patients. Remote intracerebral hemorrhage is a rare complication of craniotomy with significant morbidity and mortality.3,9 Brisman et al. reviewed 37 cases of remote POH occurring after cranial neurosurgery and concluded that such hemorrhages likely develop at or soon after surgery, tend to occur preferentially in certain locations, and can be related to the craniotomy site, operative positioning, and nonspecific mechanical factors.9 They are not related to hypertension, coagulopathy, cerebrospinal fluid drainage, or underlying pathologic abnormalities.
Analysis of Causative Factors A postoperative hematoma after elective surgery can have a devastating effect on the patient’s outcome. However, in most of the patients with POH, no obvious cause for the hematoma can be found; it is related neither to the surgical technique nor to hemostatic parameters. Various predisposing risk factors have been analyzed: Hypertension was generally found to be significant in most studies, whereas diabetes mellitus, cerebral amyloid angiopathy, and atherosclerosis were generally not significant.3,5 Basali et al. noted that patients with postoperative intracranial hemorrhage had a significantly greater rate of intraoperative and postoperative/prehemorrhage hypertension.10 Intraoperative hypertension occurs during brain manipulation, head pin application, use of epinephrine containing anesthetics, periosteal dissection, and emergence. Basali et al. also found a significantly high odds ratio for intracranial hemorrhage when patients had blood pressure <160/90 intraoperatively but then had elevated blood pressure postoperatively.10 This suggests that some vessels may not have been adequately tested intraoperatively for the possibility of leaking when blood pressure rises.10 Age is a significant risk factor for hematoma development— sixfold more likely at age over 70 and 12-fold over 75.7,11 It remains speculative why the risk of bleeding increases with age. It can be speculated that POH in the elderly is attributed to changes in the blood vessels themselves and to the function of platelets. It was found that elderly patients have more thrombin activation/ generation and fibrinolytic activity before surgery than younger patients.7 Other risk factors include antiplatelet use, including aspirin and nonsteroidal antiinflammatory drugs, preoperative mannitol administration, excessive alcohol use, coagulopathies, disseminated intravascular coagulation, thrombocytopenia, acute decreases in platelet counts postoperatively, excessive intraoperative blood loss, poor response to preoperative platelet transfusions, factor XIII deficiencies, and decreased fibrinogen levels.1–4,7 One might expect that surgeons with greater levels of experience should encounter fewer postoperative hematomas. However, in the study by Taylor et al., there was no correlation between the rank of the surgeon and the occurrence of postoperative hematoma, with 27 hematomas (54%) occurring after operations by consultants and 23 (46%) after operations by registrars or senior registrars.8
Kim et al. conclude that large intraoperative blood loss and wide craniotomy area are risk factors for postoperative EDH after intracranial surgery.12 However, this study had significant limitations because it did not examine the role of established risk factors for POH. In another series of patients, who underwent surgery to remove brain tumors, the highest rate of postoperative hematomas was found after meningioma surgery.7 POH remains a major cause of poor outcome after meningioma surgery.
Timing of Occurrence of Postoperative Hemorrhage and Overall Outcome Gerlach et al. found that the majority of their hematomas were discovered within 3 days of the initial operation.7 Kalfas and Little found that 35% of their ICH cases were discovered within 12 hours.5 Taylor et al., in their review of 2305 patients in which 50 developed postoperative hematomas, noted that 44 out of the 50 developed within 6 hours.8 What has emerged through the literature review is that there are two distinct time periods in which neurologic deterioration secondary to a hematoma occurs, the first being within 6 hours of surgery and the second being 24 hours or more from the time of surgery. The first group likely represents continued active bleeding at the operative site, and the second group represents patients in whom active bleeding is likely to have come to a halt; their clinical deterioration may represent secondary swelling and edema formation around the hematoma. Desai et al., in their review of 3109 cranial operations, noted that when the initial operation was for evacuation of intraparenchymal hematoma, the return to the operating room for evacuation of a postoperative hematoma occurred sooner than for any other type of operation.2 Generally, outcome is poor with a range of mortality from 13% to 41% depending on the type of initial operation (tumor vs traumatic ICH, etc.). Good recovery, defined as Glasgow Outcome Scale (GOS) 4 or 5, has been reported in the range of 39% to 71% of the cases in which POH developed.4−7
Strategies—Preventive and Treatment Close clinical and neurologic observations in the immediate postoperative period are the usual means of POH detection.3 Failure to adequately awaken from general anesthesia or deterioration of observation parameters would prompt for an urgent scan to check for and treat POH. Thus, our recommendations for clinical practice based on the literature reviewed would include: 1. Preoperative: Cease any antiplatelet and anticoagulant therapy for an adequate period; stop alcohol consumption; ensure platelet count, function, and coagulation parameters are normal; consider factor XIII screening; and optimize medical management of preexisting conditions, particularly hypertension. 2. Intraoperative: Avoid hypertension and excessive blood loss; replace blood losses promptly and sufficiently; aim for gross total resection of tumor wherever possible; meticulous technique and hemostasis including dural tenting, appropriate use of electrocoagulation and topical hemostats; Valsalva maneuver at the end of surgery; and a slow, gentle wean from general anesthesia. 3. Postoperative: Avoid hypertension; replace blood losses adequately; avoid upright patient positioning in the initial phase; close clinical monitoring in the first 6 h postsurgery; consider ICP monitoring or early postoperative imaging. ICP monitoring may be useful if there have been significant problems with hemostasis during surgery, if the lesion has been very vascular,
CHAPTER 7 Postoperative Hematoma in Cranial and Spinal Surgery
if blood loss has been great during surgery, or if the patient needs to remain sedated and/or ventilated after surgery.
The Spinal Perspective Symptomatic postoperative spinal epidural hematoma (SEH) is a rare, yet well-recognized, complication of spinal surgery with potentially devastating consequences.13 Some common complications, such as an incidental durotomy, have little long-term clinical impact; conversely, some rare complications, such as a clinically significant SEH, can lead to permanent neurologic deficits.14 Most patients after spinal surgery demonstrate a varying degree of epidural hematoma on imaging; however, most remain asymptomatic.13 It is therefore impractical and unnecessary to perform a postoperative MRI scan on all patients.13,14 However, prompt attention should be paid to patients who develop either new or deteriorating neurologic signs and symptoms postoperatively.15 In this section, we discuss the incidence, associated risk factors, diagnosis, and management strategies for this rare but important complication of spinal surgery.
Incidence of Postoperative Symptomatic Spinal Epidural Hematoma The actual incidence of clinically silent epidural hematoma is reported to be much higher than that found for symptomatic hematomas. Postoperative SEH is a common radiologic finding identified in 33% to 100% of surgical cases by computed tomography (CT) scan or magnetic resonance imaging (MRI).16 For example, in patients undergoing lumbar surgery, Sokolowski et al. identified a 58% incidence of asymptomatic postoperative epidural hematoma (diagnosed by MRI) compressing the thecal sac beyond its preoperative state at one or more levels.17 The majority of radiologically diagnosed SEHs are clinically silent. As per literature review, most authors define a postoperative SEH as one that is clinically symptomatic rather than one that is asymptomatic and diagnosed by radiology alone. Kao et al. reviewed over 15,500 lumbar spine surgeries and identified 25 patients with a symptomatic postoperative SEH for an incidence of 0.16%.18 Awad et al. reviewed almost 15,000 consecutive spine cases at a single institution and identified 32 cases (0.2%) of symptomatic postoperative SEH.19 In a study by Kou et al., out of approximately 12,000 spinal procedures performed over a 10-year period, 12 patients (0.1%) were identified who developed a new postoperative neurologic deficit that was surgically confirmed to be caused by a postoperative SEH.20 All cases involved lumbar laminectomies. Aono et al. reported on 6356 spinal surgeries and identified 26 (0.41%) patients with symptomatic postoperative SEH.21 The authors also identified the incidence by procedure. Zero hematomas were seen in 1568 lumbar discectomies; eight were identified in 1614 patients undergoing a lumbar laminectomy (0.5%), and eight were identified in 1191 patients undergoing a posterior lumbar interbody fusion (0.67%). As per the abovementioned articles and a detailed review of literature, the risk of a clinically significant postoperative SEH appears to be low, the range being between 0% and 1%.13,15
Risk Factors for Postoperative Spinal Epidural Hematoma The ensuing morbidity of postoperative SEH is substantial, and therefore it is a feared complication of spinal surgery.21 Identification of potentially modifiable risk factors or preventive measures is of
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value to help decrease the risk of hematoma development in this patient population.16 The rarity of this complication makes it difficult to study or draw conclusions on regarding potential predisposing risk factors. Although multiple large studies have been performed attempting to identify risk factors for this complication, there is still significant debate about the effect of subfascial drains, postoperative anticoagulation, and antiplatelet medication on the incidence of postoperative hematoma. Although there is no evidence that use of prophylactic doses of anticoagulation increases the risk of a symptomatic postoperative epidural hematoma, there is insufficient data available in the literature to define the safety profile of postoperative prophylactic anticoagulation. Kao et al. performed a case-control analysis to identify risk factors.18 Despite looking at over 20 possible risk factors including age, the use of anticoagulants, platelet count, and blood loss, the only significant risk factors for the development of a symptomatic SEH identified by the authors were an elevated preoperative diastolic blood pressure, the intraoperative use of Gelfoam for dura coverage, and high postoperative drain output. Awad et al. found the following risk factors associated with postoperative SEH: Preoperative risk factors included the use of nonsteroidal antiinflammatories, Rhpositive blood, and age above 60 years; intraoperative risk factors included surgeries involving >5 levels, significant blood loss of >1 L, and a hemoglobin of <10 g/dL; postoperative risk factors included Coumadin use only if the international normalized ratio (INR) was >2.0 in the first 48 hours.19 They also found that well-controlled anticoagulation and the use of drains were not associated with an increased risk of postoperative SEH. Kou et al. conclude that patients who require multilevel lumbar procedures and/or have a preoperative coagulopathy are at a significantly higher risk for developing a postoperative epidural hematoma. They suggest that extra precautions for meticulous hemostasis during the surgical procedure should be considered in such patients and that postoperative neurologic examinations be done routinely for them.20 Amiri et al., in their review of 4568 open spinal operations, found alcohol consumption greater than 10 units a week, multilevel procedure, and previous spinal surgery as risk factors for developing SEH.13 Studies specifically evaluating whether the presence of a postoperative subfascial drain affected the risk of symptomatic epidural hematoma have not found a significant protective effect from the use of a drain.13,19,20 Similarly, a metaanalysis looking at the effect of drain use after all orthopedic procedures found that there was no decrease in the rate of a postoperative hematoma with the use of a closed suction surgical drain.22 However, the use of a drain did lead to an increase in the need for blood transfusions. Despite the lack of evidence that subfascial drains decrease the risk of a symptomatic postoperative epidural hematoma, drains are still commonly used in lumbar spine surgery because they have been shown to decrease the risk of an asymptomatic postoperative epidural hematoma.23,24 In a prospective study in which a lumbar spine MRI was obtained on postoperative day 1 in 50 patients who underwent lumbar spine surgery, Mirzai et al. reported that the use of a drain significantly decreased the incidence of an asymptomatic epidural hematoma from 89% to 36%.24 Importantly, none of the patients in either of these studies had evidence of neurologic deficit related to the epidural hematomas.
Diagnosis and Management of Symptomatic Postoperative Spinal Epidural Hematoma Once SEH has occurred, it is important to act rapidly to minimize any lasting disability. Delay in surgical evacuation has previously
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SE C T I O N 1
General Neurosurgery
resulted in a successful litigation case.13 Almost all patients who develop a symptomatic postoperative epidural hematoma have some evidence of neurologic compromise.14 The symptoms of SEH usually occur within 24 hours after the initial surgery.18,21 Kao et al. reported that 80% of patients with a lumbar epidural hematoma presented with progressive loss of postoperative muscle strength, 76% presented with some amount of saddle anesthesia, and 56% presented with a sudden severe increase in pain.18 When any of these symptoms are present, the patient should undergo an emergent MRI to evaluate for a possible epidural hematoma. It is preferred to obtain an MRI on all patients with new neurologic findings postoperatively to ensure that the diagnosis of a postoperative SEH is not missed or delayed. Most authors agree that emergent surgical evacuation should be performed as soon as possible when neurologic deterioration is detected and postoperative SEH is suspected.14,15,25 Delamarter et al. have demonstrated, in a model of dogs, that recovery from spinal cord compression is inversely associated with duration of compression, and that demyelination after compression occurs in direct proportion to the duration of compression.26 Kebaish and Awad concluded that if patients undergo evacuation operation within 6 hours of symptom onset of postoperative deficit, the neurologic outcomes are usually better.27 In a study of 30 cases of epidural hematoma with neurologic deficit due to various causes such as spinal surgery and anticoagulation medications, Lawton et al. revealed that the rapidity of taking patients to re-operation correlated with better neurological outcomes.25 Hence, symptomatic postoperative SEH should be suspected in any patient with a new-onset neurologic deterioration in the postoperative period; the patient should be diagnosed with an MRI or CT (if urgent neuroimaging is possible), and an emergent decompression surgery should be performed as early as possible.
Conclusion “A stitch in time saves nine.” POH in neurosurgery is a harbinger of poor neurologic outcome and hence should be given due importance. It is imperative to check hemodynamic and coagulation factors before taking up a patient for any neurosurgical procedure. However, the truth of the matter is that even after doing everything right both preoperatively and intraoperatively, POH can occur even in the absence of any risk factors. The neurosurgeon always has to be vigilant toward this dreaded complication. An examination/imaging study in time saves the patient valuable neurons and significantly improves the overall outcome.
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