Spectrum of remote site extradural hematomas following decompressive craniectomy: Does fracture always co-exist?
- Department of Neurosurgery, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
- Department of Neurosurgery, Dayanand Medical College and Hospital, Ludhiana, Punjab, India.
Madhivanan Karthigeyan, Department of Neurosurgery, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
DOI:10.25259/SNI_484_2021Copyright: © 2021 Surgical Neurology International This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.
How to cite this article: Apinderpreet Singh1, Chetan Wadhwa2, Madhivanan Karthigeyan1, Pravin Salunke1, Hanish Bansal2, Ashwini Kumar Chaudhary2. Spectrum of remote site extradural hematomas following decompressive craniectomy: Does fracture always co-exist?. 06-Sep-2021;12:443
How to cite this URL: Apinderpreet Singh1, Chetan Wadhwa2, Madhivanan Karthigeyan1, Pravin Salunke1, Hanish Bansal2, Ashwini Kumar Chaudhary2. Spectrum of remote site extradural hematomas following decompressive craniectomy: Does fracture always co-exist?. 06-Sep-2021;12:443. Available from: https://surgicalneurologyint.com/surgicalint-articles/11097/
Background: Remote-site extradural hematomas (EDHs) after decompressive-surgeries for traumatic brain injury (TBI) are rarely encountered. Typically, they form contralateral to the injured side, with an overlying fracture. We present a subset which developed EDH immediately after decompressive-hemi-craniectomy for TBI, most without an evidence of fracture, and not limited to contralateral location.
Methods: Nine such patients were retrospectively identified. Plausible mechanisms, management issues and outcomes have been discussed.
Results: All nine patients were victims of severe-TBI. Six did not have any skull-fractures. Eight showed hemispheric-injuries while one had bifrontal-contusions. In hemispheric-injuries, midline-shift was at least 8 mm except one with midline-shift of 6 mm. The EDH was straddling the midline in 2 (bifrontal-1, bi-occipital-1), and juxtaposed to the previous craniectomy in 1, apart from a contralateral-bleed in 6; all, except one, needed evacuation. In most patients, venous-source of bleed was identified. All had improved from their preoperative Glasgow coma scale (GCS) at follow-up.
Conclusion: A fracture need not always co-exist in EDH following decompressive craniectomy. However, an extra-caution is suggested in its presence. Given the need for surgical-evacuation in most patients and an inability to assess immediate postoperative-GCS in severely head-injured, a routine postoperative-computed tomography is recommended to avoid overlooking such potentially treatable condition.
Keywords: Decompressive hemicraniectomy, Extradural hematoma, Head injury, Traumatic brain injury
Development of remote site extradural hematoma (EDH) following decompressive hemicraniectomies for traumatic brain injury (TBI) is a rare but potentially devastating complication with reported incidence in the range of 5–12%.[
We present the clinical experience of a series of patients with remote site EDH post decompressive status, the majority of which did not show any fracture and not strictly contralateral, yet developed such complication. In this article, we attempted to analyze the following features of this infrequently encountered entity by keeping in mind three research questions: (1) do the hematomas always occur contralateral to the craniotomy site? (2) Is presence of an overlying fracture mandatory for such bleeds? and (3) Do all patients need evacuation?
Ours is a retrospective, hospital-based, and observational study. After obtaining institutional ethical clearance, the data of patients who developed remote site EDH after decompressive hemicraniectomies for various TBIs between the period 2015 and 2019 were retrieved from the hospital records.
Clinical and radiological data
Patients’ demographic details, modes of injury, preoperative Glasgow coma scale (GCS), and injury pattern for which the decompressive surgery was performed were noted. These patients neither had any associated coagulopathy or thrombocytopenia nor were on anticoagulant/antiplatelet medications. Furthermore, they did not carry any other comorbidity with bleeding diathesis.
Their preoperative computed tomography (CT) was evaluated for location and type of injury, extent of mass effect (midline shift and effacement of cisterns), Rotterdam score and presence of fracture at a remote site.[
Surgical data and postoperative protocols
The operative records of patients were looked for the presence of any significant brain bulge during surgery. All the patients underwent surgery with their head positioned on a head-ring; no skull clamps were used. A fronto-temporo-parietal craniectomy with loose duraplasty was performed, and the size of the bone flap was almost similar (approximately 15*12 cm) in all cases.
As a standard operating protocol, we routinely performed postoperative CT scans within an hour in all the patients. Furthermore, those with severe TBI or significant brain edema were shifted unreversed to our intensive care facility and electively ventilated. Hence, the interval GCS of these patients was not known.
Management of postoperative remote site EDH
A decision to operate upon the postoperative EDH depended on its size and the mass effect it produced. Patients who did not require an immediate clot evacuation were followed-up with serial scans and close observation of their clinical status; routine monitoring of intracranial pressure (ICP) was not a part of TBI management protocol in our set-up and was not performed. Their details such as location of bleed on CT, operative findings at second surgery, GCS at discharge, and Glasgow outcome score (GOS) at follow-up were noted.
A total of 9 (0.4%) were found to have remote side EDH after decompressive surgery performed for 2108 patients with TBI. [
Baseline preoperative findings
The age varied between 22 and 55 years (mean, 34 years). There were seven males and two females. All patients had severe head injury (GCS ≤8) secondary to motor vehicular accidents.
Of the nine patients, eight sustained hemispheric injuries, and one had bilateral frontal contusions. Among the patients with hemispheric injuries, seven showed complete effacement of cisterns (midline shift of 8–10 mm) and one had partially effaced cisterns (midline shift of 6 mm). The patient with bilateral frontal contusions showed chinking of ventricles with effacement of the basal cisterns. The Rotterdam score was measured as 5 in 7 (77.8%), and 4 in 2 patients (22.3%).
Of the nine patients, 6 (66.7%) had no associated skull fractures whereas 3 (33.3%) had evidence of fracture. In the latter, two patients had fracture at contralateral site, and one adjacent to the site of contusion.
Intra-operative findings at initial surgery
At surgery, persistent brain bulge was noticed in all even after removal of the post traumatic lesions (SDH/contusions).
Postoperative CT findings
Of 9 patients, the EDH was contralateral to the craniotomy site in six patients [
(Contralateral EDH with fracture) (a) Preoperative CT shows right frontotemporal acute SDH with midline shift, and contralateral frontotemporal linear fracture (arrow). (b) Postoperative CT shows huge contralateral EDH underneath the fracture. (c) Repeat CT postevacuation; however, the patient developed right posterior cerebral artery infarct. EDH: Extradural hematomas, SDH: Subdural hematomas, CT: Computed tomography.
(Contralateral EDH without fracture). (a) Baseline CT shows left hemispheric SDH with mass effect. (b) Postoperative CT following decompressive craniectomy shows left sided blossoming contusions, and newly developed large contralateral EDH. EDH: Extradural hematomas, SDH: Subdural hematomas, CT: Computed tomography.
(Contralateral EDH without fracture) (a) Preoperative CT shows left fronto-temporo-parietal acute SDH and underlying contusions with mass effect and completely effaced cisterns. (b) Postoperative CT shows contralateral small right frontal EDH; the patient was managed conservatively. EDH: Extradural hematomas, SDH: Subdural hematomas, CT: Computed tomography.
(Bifrontal EDH without fracture). (a) Preoperative CT shows left hemispheric SDH with underlying contusions, subarachnoid bleed and the presence of severe midline shift. (b) Postdecompression scan shows freshly formed bifrontal EDH. EDH: Extradural hematomas, SDH: Subdural hematomas, CT: Computed tomography.
Intra-operative findings at 2nd surgery
All the patients required surgical evacuation except one who had a small frontal EDH which was managed conservatively [
Postoperative course and outcome
At discharge, all the patients showed improvement from their preoperative status. At the 6-month follow-up, three patients remained in persistent vegetative state (GOS, 2), five had severe disability (GOS, 3), and one was moderately disabled (GOS, 4).
Formation of remote site hemorrhage has been described after intracranial procedures, performed for both traumatic and non-traumatic causes.[
Postoperative EDH after decompressive craniectomies for TBI can present immediately or in delayed fashion (hours to few days).[
In the previous studies, certain predictors of postoperative EDH have been reported, the most important of which is the presence of skull fractures [
In prior reports, linear fracture in association with an EDH has been observed in about 80% of cases.[
As in previous studies, an evidence of an increasing mass effect on CT/Rotterdam score corresponded to development of postsurgical EDH.[
A couple of patients in the present series developed midline EDH. The likely source of hemorrhage was venous rupture because of the stretch of the diploic/bridging veins at their entry into the dural venous sinuses. Dural sinus thrombosis as a cause of spontaneous EDH has also been reported, and can occur even in the absence of an overlying fracture.[
One of our patients developed EDH who presented adjacent to the previous craniectomy defect. Excessive stripping of dura during its separation around the burr holes can predispose to such bleed at the proximity of the craniectomy.
The commonly used hitch sutures can limit relatively small EDH between the adjacent bone and stripped dura. However, when the dura is inadvertently stripped to a large extent, these sutures per se can compartmentalize the hematoma which subsequently can evolve.
Rarely, EDH related to the pin site of the skull clamps has been reported.[
Because abrupt decompression is considered the inciting event in the origin of contralateral EDH, previous authors have suggested certain precautionary measures for a gradual reduction in ICP.[
A high index of suspicion is the only key to identify new-onset contralateral extradural bleed following decompressive craniectomy. Persistent raised ICP in the postoperative period indicated by a clinical examination (hypertension and bradycardia) can clue this unprecedented complication. Such contralateral EDH phenomenon reiterates the importance of postoperative routine ICP monitoring and a thorough neurological assessment in the neuro-intensive care unit for new onset anisocoria.[
The study is limited by its retrospective nature. Another limitation is a less number of patients because of which statistical derivations could not be drawn.
In summary, the subset of patients in this series comprised TBI patients who developed postoperative EDH at various sites, predominantly without any associated fracture. Increased mass effect and brain bulge during surgery can possibly predict such a complication. Although the occurrence of remote site EDH may be infrequent, the only way to pick up these potentially treatable lesions is by performing immediate routine postoperative CT, at least in severely head injured patients.
The procedures performed were in accordance with the ethical standards of the institutional ethics committee and with the 1964 Helsinki declaration and its later amendments. For this, type of study formal consent is not required.
Institutional Review Board (IRB) permission obtained for the study.
There are no conflicts of interest.
1. Boviatsis EJ, Korfias S, Kouyialis AT, Sakas DE. Epidural haematoma after evacuation of contralateral subdural haematoma. Ir J Med Sci. 2004. 173: 217-8
2. Chen J, Li M, Chen L, Chen W, Zhang C, Feng Y. The effect of controlled decompression for severe traumatic brain injury: A randomized, controlled trial. Front Neurol. 2020. 11: 107
3. Doddamani RS, Sawarkar D, Meena RK, Gurjar H, Singh PK, Singh M. Remote cerebellar hemorrhage following surgery for supratentorial lesions. World Neurosurg. 2019. 126: e351-9
4. Feuerman T, Wackym PA, Gade GF, Lanman T, Becker D. Intraoperative development of contralateral epidural hematoma during evacuation of traumatic extraaxial hematoma. Neurosurgery. 1988. 23: 480-4
5. Flordelís Lasierra JL, Fuentes CG, Vázquez DT, Fernández MC, Aznárez SB, López EA. Contralateral extraaxial hematomas after urgent neurosurgery of a mass lesion in patients with traumatic brain injury. Eur J Trauma Emerg Surg. 2013. 39: 277-83
6. Ganau M, Ligarotti GK, Apostolopoulos V. Real-time intraoperative ultrasound in brain surgery: Neuronavigation and use of contrast-enhanced image fusion. Quant Imaging Med Surg. 2019. 9: 350-8
7. Ganau M, Prisco L. Comment on. “neuromonitoring in traumatic brain injury”. Minerva Anestesiol. 2013. 79: 310-11
8. Kim SH, Lee JH, Joo W, Chough CK, Park HK, Lee KJ. Analysis of the risk factors for development of post-operative extradural hematoma after intracranial surgery. Br J Neurosurg. 2015. 29: 243-8
9. Knopman J, Tsiouris AJ, Souweidane MM. Atraumatic epidural hematoma secondary to a venous sinus thrombosis: A novel finding. J Neurosurg Pediatr. 2008. 2: 416-9
10. Matsuno A, Katayama H, Wada H, Morikawa K, Tanaka K, Tanaka H. Significance of consecutive bilateral surgeries for patients with acute subdural hematoma who develop contralateral acute epi-or subdural hematoma. Surg Neurol. 2003. 60: 23-30
11. Oh MJ, Jeong JH, Shin DS, Hwang SC, Im SB, Kim BT. Postoperative contralateral hematoma in patient with acute traumatic brain injury. Korean J Neurotrauma. 2017. 13: 24-8
12. Picetti E, Caspani ML, Iaccarino C, Pastorello G, Salsi P, Viaroli E. Intracranial pressure monitoring after primary decompressive craniectomy in traumatic brain injury: A clinical study. Acta Neurochir (Wien). 2017. 159: 615-22
13. Piepmeier JM, Wagner FC. Delayed post-traumatic extracerebral hematomas. J Trauma. 1982. 22: 455-60
14. Saberi H, Meybodi AT, Meybodi KT, Habibi Z, Mirsadeghi SM. Delayed post-operative contralateral epidural hematoma in a patient with right-sided acute subdural hematoma: A case report. Cases J. 2009. 2: 6282
15. Shen J, Pan JW, Fan ZX, Zhou YQ, Chen Z, Zhan RY. Surgery for contralateral acute epidural hematoma following acute subdural hematoma evacuation: Five new cases and a short literature review. Acta Neurochir (Wien). 2013. 155: 335-41
16. Stiver SI. Complications of decompressive craniectomy for traumatic brain injury. Neurosurg Focus. 2009. 26: E7
17. Su TM, Lan CM, Lee TH, Hsu SW, Lu CH. Risk factors for the development of contralateral epidural hematoma following decompressive craniectomy in patients with calvarial skull fracture contralateral to the craniectomy site. World Neurosurg. 2016. 89: 223-9
18. Su TM, Lee TH, Chen WF, Lee TC, Cheng CH. Contralateral acute epidural hematoma after decompressive surgery of acute subdural hematoma: Clinical features and outcome. J Trauma. 2008. 65: 1298-302
19. Talbott JF, Gean A, Yuh EL, Stiver SI. Calvarial fracture patterns on CT imaging predict risk of a delayed epidural hematoma following decompressive craniectomy for traumatic brain injury. AJNR Am J Neuroradiol. 2014. 35: 1930-5
20. Yan HJ. Epidural hematoma following use of a three-point skull clamp. J Clin Neurosci. 2007. 14: 691-3