TO THE EDITOR: We read the article by Peres et al.6 with great interest (Peres CMA, Caldas JGMP, Puglia P Jr, et al: Endovascular management of acute epidural hematomas: clinical experience with 80 cases. J Neurosurg [epub ahead of print April 14, 2017. DOI: 10.3171/2016.11.JNS161398]). In this paper, the authors analyzed the safety and efficacy of embolization of the involved middle meningeal artery (MMA) and associated lesions in small- to medium-sized acute epidural hematomas (EDHs). They had treated 80 patients with small- to medium-sized EDHs using embolization of the MMA and its associated lesions. They compared their results with those in a historical cohort of 471 patients. After embolization of the MMA, there was no increase in the size of the EDH in any of the 80 patients in their study. They concluded that embolization is a highly effective and safe method for achieving size stability in nonsurgically treated acute EDHs. We congratulate the authors for considering endovascular treatment for small EDHs and thus avoiding an increase in the size of the lesions, repeated scans, and prolonged hospital stays. However, we would like to draw the reader’s attention to a few pertinent points.
In their study, the authors mentioned that the mean and median durations from admission to angiography were 4.6 and 4 days, respectively. It has been concluded in various studies that an increase in the size of EDH usually occurs within 24 hours.8–10 Sakai et al. demonstrated that small EDHs (65%) expanded in the 24 hours after trauma.8 Sullivan et al. found that 25% of EDHs enlarged in the first 24 hours.9 In a study by Knuckey et al., 22% of patients deteriorated within 24 hours and only 1 patient deteriorated after 10 days.4 In a study by Basamh et al., 11.2% patients deteriorated in a mean range of 5–30 hours.1 Progression of initially nonsurgically treated EDHs mostly occurs within the first 24 hours, is less likely within 48 hours, and rarely occurs beyond that.1 In the study by Peres et al., endovascular intervention was performed at a mean duration of 4.6 days, after which enlargement of EDH is rare. The authors did not include the time period from the time of injury to admission, which further increases the interval between trauma and intervention. Hence, it would not be appropriate to conclude that the EDH did not increase in size because of the endovascular therapy. Moreover, the utility of embolization in these cases in terms of preventing the need of surgery cannot be concluded until a case controlled trial is done.
Suzuki et al.10 showed that endovascular intervention is useful in patients with active contrast extravasation and an increase in the size of a hematoma. Only 61 patients had contrast extravasation in the study by Peres et al., but they did not mention an increase in the size of EDH. Although there is a theoretical risk of bleeding from a pseudoaneurysm, the usefulness of embolization in small EDHs cannot be commented on until the natural history of these lesions is known.2
In the study by Peres et al., 6 patients with normal angiographic findings, 8 patients with MMA wall irregularities, and 1 patient with choroidal blush and an internal carotid artery aneurysm each underwent embolization. The authors did not mention the reasons for embolization in these patients.
We agree with the authors that endovascular embolization is a safe and efficient method, but one cannot conclude that it is effective in preventing the morbidity and mortality associated with small EDHs until the natural history of these lesions is known and embolization is performed early and the intervention group is compared with a nonintervention group. We also believe that endovascular intervention is an excellent tool especially for controlling torrential bleeding from the MMA intraoperatively, in severely comorbid patients, and in cases of multiple lesions.3,5,7 It can be selectively done in patients with risk factors such as unstable EDH, active contrast extravasation, fracture running across the MMA, and enhancement of hematomas on MRI.11
Disclosures
The authors report no conflict of interest.
References
- 1↑
Basamh M, Robert A, Lamoureux J, Saluja RS, Marcoux J: Epidural hematoma treated conservatively: when to expect the worst. Can J Neurol Sci J Can Sci Neurol 43:74–81, 2016
- 2↑
de Andrade AF, Figueiredo EG, Caldas JG, Paiva WS, De Amorim RLO, Puglia P, et al.: Intracranial vascular lesions associated with small epidural hematomas. Neurosurgery 62:416–421, 2008
- 3↑
Kim MH: Transcortical endoscopic surgery for intraventricular lesions. J Korean Neurosurg Soc 60:327–334, 2017
- 4↑
Knuckey NW, Gelbard S, Epstein MH: The management of “asymptomatic” epidural hematomas. A prospective study. J Neurosurg 70:392–396, 1989
- 5↑
Ohshima T, Tajima H, Fujii K, Nagakura M, Nishizawa T, Kato K, et al.: Combined endovascular and endoscopic surgery for acute epidural hematoma in a patient with poor health. Neurol Med Chir (Tokyo) 52:829–831, 2012
- 6↑
Peres CMA, Caldas JGMP, Puglia P Jr, de Andrade AF, da Silva IAF, Teixeira MJ, et al.: Endovascular management of acute epidural hematomas: clinical experience with 80 cases. J Neurosurg [epub ahead of print April 14, 2017. DOI: 10.3171/2016.11.JNS161398]
- 7↑
Ross IB: Embolization of the middle meningeal artery for the treatment of epidural hematoma. J Neurosurg 110:1247–1249, 2009
- 8↑
Sakai H, Takagi H, Ohtaka H, Tanabe T, Ohwada T, Yada K: Serial changes in acute extradural hematoma size and associated changes in level of consciousness and intracranial pressure. J Neurosurg 68:566–570, 1988
- 9↑
Sullivan TP, Jarvik JG, Cohen WA: Follow-up of conservatively managed epidural hematomas: implications for timing of repeat CT. AJNR Am J Neuroradiol 20:107–113, 1999
- 10↑
Suzuki S, Endo M, Kurata A, Ohmomo T, Oka H, Kitahara T, et al.: Efficacy of endovascular surgery for the treatment of acute epidural hematomas. AJNR Am J Neuroradiol 25:1177–1180, 2004
- 11↑
Tomida M, Muraki M, Uemura K, Yamasaki K: Postcontrast magnetic resonance imaging to predict progression of traumatic epidural and subdural hematomas in the acute stage. Neurosurgery 43:66–71, 1998
