Craniotomy for Treatment of Chronic Subdural Hematoma




Chronic subdural hematomas are commonly encountered pathologies in neurologic surgery. Primary management for a symptomatic lesion usually entails surgical intervention. There is controversy regarding ideal modality selection among twist drill craniostomy, bur hole craniostomy, and craniotomy. Variations of the craniotomy include a minicraniotomy (usually defined as 30–40 mm diameter), minicraniectomy, and with or without either a partial or full membranectomy. In addition to medical complications, potential surgical complications include recurrence, seizures, intraparenchymal hemorrhage, and infection. Prior studies are summarized as well as rates of mortality, morbidity, reaccumulation requiring repeat operation, and clinical outcomes.


Key points








  • Surgical intervention for chronic subdural hematomas (cSDHs) should be considered in cases of failed medical/conservative management or radiographic progression or with evidence of neurologic symptoms or deficit.



  • Burr hole craniostomy (BHC) remains the gold standard for initially approaching cSDH, especially if liquefied and nonseptated.



  • Craniotomy is particularly useful in treating cSDHs in cases of recurrence or with radiographic evidence of membranes.



  • Craniotomy is associated with a higher morbidity and mortality than BHC and twist drill craniostomy (TDC), although with a lower complication rate than BHC and rates of recurrence similar to TDC.



  • There is no reliably proved advantage to performing an aggressive total membranectomy.






Introduction


cSDHs are one of the more commonly encountered pathologies in neurologic surgery, with an estimated incidence of 1 to 2 in 100,000, a predilection for the elderly with a male predominance, and a predicted rise in incidence secondary to increasing life expectancy in developed countries. Risk factors include a history of trauma, alcohol abuse, seizures, the presence of cerebrospinal fluid diversion (ie, ventriculoperitoneal shunt), and coagulopathies or anticoagulation. The underlying pathophysiology likely relates to an inflammatory process in the dura mater and subdural space in response to acute hemorrhage or some other insult. Subsequent neovascularization, formation of macrocapillaries, and vascular hyperpermeability lead to exudation and can contribute to hematoma enlargement, and higher rates of exudation have been correlated with worse clinical status. The major culprit behind hematoma enlargement, however, remains the microhemorrhages associated with rupture of the fragile vessels generated with neovascularization. The natural history of cSDH depends largely on patient-specific conditions, although spontaneous resolution is possible. Clinical severity of cSDH can be quantified with the Markwalder grading system ( Table 1 ). Radiographically, cSDH can be categorized into 1 of 5 categories based on CT imaging characteristics, as proposed in the Nomura classification system, including (1) high density, (2) isodensity, (3) low density, (4) mixed density, and (5) layering lesions. Primary management for a symptomatic lesion is usually with surgical intervention, via (1) TDC – which can be done under local anesthetic in cases of medically complex patients, (2) BHC, or (3) craniotomy bone flap (ie, >30 mm), although medical use of dexamethasone in some patients is a viable option used in international case series with comparable clinical outcomes. There are several variations with craniotomy that are used, including a minicraniotomy (usually defined as 30–40 mm diameter), minicraniectomy, and either partial or full membranectomy. The goal of this article is to discuss the role of craniotomy in treating cSDH.



Table 1

Markwalder scale for grading clinical condition in chronic subdural hematoma


















Grade 0 No neurologic deficits
Grade 1 Mild symptoms (ie, headache, absent or mild neurologic deficits like reflex asymmetry)
Grade 2 Drowsiness or disoriented with variable neurologic deficit (ie, hemiparesis)
Grade 3 Stupor, severe focal neurologic deficit (ie, hemiplegia)
Grade 4 Coma, posturing, or absence of motor response to noxious stimulation

From Markwalder TM, Steinsiepe KF, Rohner M, et al. The course of chronic subdural hematomas after burr-hole craniostomy and closed-system drainage. J Neurosurg 1981;55(3):390–6; with permission.




Introduction


cSDHs are one of the more commonly encountered pathologies in neurologic surgery, with an estimated incidence of 1 to 2 in 100,000, a predilection for the elderly with a male predominance, and a predicted rise in incidence secondary to increasing life expectancy in developed countries. Risk factors include a history of trauma, alcohol abuse, seizures, the presence of cerebrospinal fluid diversion (ie, ventriculoperitoneal shunt), and coagulopathies or anticoagulation. The underlying pathophysiology likely relates to an inflammatory process in the dura mater and subdural space in response to acute hemorrhage or some other insult. Subsequent neovascularization, formation of macrocapillaries, and vascular hyperpermeability lead to exudation and can contribute to hematoma enlargement, and higher rates of exudation have been correlated with worse clinical status. The major culprit behind hematoma enlargement, however, remains the microhemorrhages associated with rupture of the fragile vessels generated with neovascularization. The natural history of cSDH depends largely on patient-specific conditions, although spontaneous resolution is possible. Clinical severity of cSDH can be quantified with the Markwalder grading system ( Table 1 ). Radiographically, cSDH can be categorized into 1 of 5 categories based on CT imaging characteristics, as proposed in the Nomura classification system, including (1) high density, (2) isodensity, (3) low density, (4) mixed density, and (5) layering lesions. Primary management for a symptomatic lesion is usually with surgical intervention, via (1) TDC – which can be done under local anesthetic in cases of medically complex patients, (2) BHC, or (3) craniotomy bone flap (ie, >30 mm), although medical use of dexamethasone in some patients is a viable option used in international case series with comparable clinical outcomes. There are several variations with craniotomy that are used, including a minicraniotomy (usually defined as 30–40 mm diameter), minicraniectomy, and either partial or full membranectomy. The goal of this article is to discuss the role of craniotomy in treating cSDH.



Table 1

Markwalder scale for grading clinical condition in chronic subdural hematoma


















Grade 0 No neurologic deficits
Grade 1 Mild symptoms (ie, headache, absent or mild neurologic deficits like reflex asymmetry)
Grade 2 Drowsiness or disoriented with variable neurologic deficit (ie, hemiparesis)
Grade 3 Stupor, severe focal neurologic deficit (ie, hemiplegia)
Grade 4 Coma, posturing, or absence of motor response to noxious stimulation

From Markwalder TM, Steinsiepe KF, Rohner M, et al. The course of chronic subdural hematomas after burr-hole craniostomy and closed-system drainage. J Neurosurg 1981;55(3):390–6; with permission.




Methods


The authors systematically reviewed the literature, using PubMed, with the search terms “chronic subdural hematoma”, “craniotomy”, and “outcomes”. Any studies with only TDC or BHC as a surgical intervention or articles that combined outcomes of craniotomy with another subgroup were excluded. Non-English articles were also excluded. Patient cohort details, mortality, clinical outcomes, recurrence rate, and complication rates were documented for each study. Risk factors for either “poor” clinical outcomes or recurrence requiring operative intervention were documented as well as each group’s specific definition of “poor outcome.” Finally, the authors’ institutional philosophy for triage of cSDH, surgical design, patient selection, and details of operation for performing a craniotomy were reviewed.




Indications/contraindications


Indications for craniotomy include any sort of symptomatic clot or fluid collection (ie, focal neurologic deficit related to the clot), with or without failed conservative or less invasive (ie, BHC) management. Possible symptoms include headache, nausea or vomiting, seizures (either focally related to clot or generalized), weakness or numbness contralateral to the lesion, and aphasia for lesions on the dominant hemisphere. Evidence of the radiographic progression during a course of conservative observation is also a reasonable indication for consideration of operative intervention.


The selection of surgical technique is a topic of debate and unfortunately largely understudied; a recent systematic review published by Ivamoto and colleagues identified 24 randomized controlled trials (RCTs) in the surgical management of cSDHs, including comparisons, such as using a subdural drain postoperatively or using 1 versus 2 burr holes. The only RCT associated with craniotomy compared it to medical management with mannitol, and the trial was aborted after the first 7 patients in the medical arm had to cross over to the surgical arm. It is generally a reasonable strategy to approach cSDH with BHC initially, because this procedure seems to achieve an ideal balance of limiting complications, mortality, and recurrence compared with TDC and craniotomy. Still, surgeons should consider craniotomy in cases of (1) recurrence despite prior surgical intervention or (2) clots with evidence of membranes, which might inhibit evacuation via burr holes. Some investigators argue for performing contrasted MRI preoperatively, because this can highlight membranes and define particular cases where craniotomy may be useful as an upfront modality. Fig. 1 depicts a theoretical example of different membrane organization and triage strategy; in a study by Tanikawa and colleagues,27 patients with “type C” membranes (ie, extensive and multilayered on T2 MRI) treated with BHC had longer hospital stays, higher re-operation rates, and worse neurological outcomes compared to those treated with craniotomy. Fig. 2 demonstrates an example of a mixed subacute/chronic SDH approached with craniotomy as an initial strategy given radiographic evidence of significant membranes.




Fig. 1


Schema of intrahematomal structure as depicted by T2-weighted MRI. Left side of figure depicts a type B hematoma without any intrahematomal membrane. Middle of figure shows a type B hematoma with a monolayer multilobule hematoma. Right side of figure shows a type C hematoma, with a multilayer hematoma.

( From Tanikawa M, Mase M, Yamada K, et al. Surgical treatment of chronic subdural hematoma based on intrahematomal membrane structure on MRI. Acta Neurochir (Wien) 2001;143:613–9; with permission.)



Fig. 2


Example of cSDH treated with craniotomy upfront. ( A,B ) Pre-operative head CT, demonstrating evidence of membranous subdural clot, mixed density, with local mass effect (axial and coronal cuts, respectively). ( C,D ) Post operative head CT demonstrating effective clot evacuation (axial and coronal cuts, respectively). ( E ) 6 week follow up head CT demonstrating persistent treatment (axial cut). ( F ) Lateral skull film demonstrating the extent of craniotomy.




Surgical technique


Preoperative Planning


Preoperatively, patients with either frank seizures or clinical behavior suspicious for seizures (ie, intermittent weakness or aphasia) should be loaded and maintained on an antiepileptic drug (AED) regimen appropriate to seizure type, although if seizure symptomatology is mild, it is sometimes reasonable to give surgical intervention an opportunity for relieving seizures, in which case AEDs can be avoided completely. If admitted through an emergency department, patients can be monitored on the normal wards (ie, infrequent neurochecks) with a nonemergent surgical plan unless there is significant mass effect, focal neurologic deficits, or severe symptoms. Emergent intervention should be considered in the event of new neurologic deficits, like weakness, because these can be permanent and due to vascular compression from mass effect. Basic preoperative laboratory tests should be obtained, and any coagulopathies should be corrected prior to surgical intervention. For patients on aspirin, the authors typically administer 1 U of platelets at the time of skin incision and plan to hold the medication anywhere from 48 hours to 2 weeks postoperatively, depending on the indication. The authors treat preoperative Coumadin/anticoagulation with fresh frozen plasma reversal and hold the medication in a similar time frame as for aspirin.


In reviewing imaging, coronal reformats of head CT are particularly useful for planning craniotomy, especially in cases of minicraniotomy planned. Identification of the superior temporal line is useful to estimate cranial and caudal extension and extent of craniotomy in that plane, whereas identification of the clot in relation to the external auditory meatus helps to define the anterior and posterior boundaries.


Patient Positioning


Patients are positioned supine, with all pressure points padded appropriately and a shoulder bump under the ipsilateral side to promote exposure of the calvarium of the operative side. Either a horseshoe head-holder or Mayfield 3-point pin fixation can be used, although the authors’ preference with any craniotomy is the latter. Attention is directed toward preoperative imaging to ensure that pins are not placed into the frontal sinus, and deliberate care is directed toward exposing a full calvarium for surgical preparation in the rare but potentially hazardous situation where conversion to a full-sized trauma-style craniotomy is necessary (ie, exposure of the zygomatic process, significant posterior extension into the occipital region, medial to the midline, and anterior up to the forehead). The head is slightly turned but without any kinking of the neck both for airway stability and to ensure proper venous drainage through the jugular veins. A curvilinear incision is planned along the theoretic blueprint of a trauma-style, reverse-question-mark incision. Alternatively, if a larger craniotomy is planned, a full or mini reverse-question-mark style incision can be planned.


Surgical Procedure


After exposing the calvarium, 1 or 2 burr holes are fashioned along the borders of the craniotomy. A Penfield #3 is used to strip the dura from the inner surface of bone prior to using the craniotome to fashion the craniotomy. Care should be taken to not extend the craniotomy over the superior sagittal sinus nor tear the dura along the medial border of the bony exposure to avoid cortical venous injury. Epidural tack-up stitches are placed with 4-0 neurolon stitches along the perimeter of the craniotomy. The dura is opened in a cruciate or stellate fashion. It is not necessary to identify the entire perimeter of the membrane/clot, because a full membranectomy is not essential. The outer layer of the membrane is entered and gently irrigated, because the boundaries are explored up until the perimeter of the craniotomy. Gentle irrigation of the inner, cortical membrane layer can be performed, although aggressive traction and resection are not advised, because there can be adhesions to the cortical brain surface/veins, and these can cause new hemorrhage. All visible membrane (outer layer) is coagulated with bipolar cautery, including just under the edges of the craniotomy. When hemostasis is achieved, the bone flap is replaced with titanium plates and screws. The authors do not place any dural substitute over the cavity or close the dura tightly, because this promotes an outlet for subdural drainage via a subgaleal drain.




Potential complications and management


Postoperative complications related to craniotomy for cSDH can be grouped into medical complications related to hospitalization and more surgically specific complications. Medical complications are more common than surgical ones, partially owing to older, medical complicated typical cSDH patients. Rates are intermittently reported in various series and include urinary tract infection, pneumonia, deep venous thrombosis with or without pulmonary embolus, myocardial infarction, pneumothorax, stroke, and so forth. Higher rates of complication seem to be associated with longer hospital stays and more extensive preoperative medical comorbidities, although formal validation in the cSDH population remains to be demonstrated. Table 2 summarize the existing studies in the literature with craniotomy as compared to other treatment modalities for cSDH, with the various outcomes assessed, and rates of complication, mortality, morbidity, recurrence, and “good” clinical outcomes. Table 2 lists the rates of surgical complications reported in various series in the literature; reported rates range from 0% to 44.8%, including new onset of seizures, intraparenchymal hemorrhage, wound infection, and development of a subdural empyema. Again, a more recent meta-analysis suggests the rate of complication is likely in the range of 10.2% to 12.6%. Thirty-day mortality rates are also reported in Table 2 , with rates ranging from 0% to 20%, and all cases being unrelated to intracranial pressure, focal neurologic issues, or subdural recurrence. Based on more recent and statistically elegant analyses, the actual mortality is probably closer to 4% to 6.8%.


Oct 12, 2017 | Posted by in NEUROSURGERY | Comments Off on Craniotomy for Treatment of Chronic Subdural Hematoma

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