http://informahealthcare.com/bij ISSN: 0269-9052 (print), 1362-301X (electronic) Brain Inj, Early Online: 1–4 ! 2014 Informa UK Ltd. DOI: 10.3109/02699052.2014.990513

ORIGINAL ARTICLE

Chronic subdural haematoma evolving from traumatic subdural hydroma Yaodong Wang1,2, Chuanwei Wang1, & Yuguang Liu1,3 Department of Neurosurgery, Qilu Hospital of Shandong University, Jinan, PR China, 2Third Affiliated Hospital of Liaoning Medical University, Jinzhou, PR China, and 3Brain Science Research Institute of Shandong University, Jinan, PR China

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Abstract

Keywords

Objective: This study aimed to investigate the incidence and clinical characteristics of chronic subdural haematoma (CSDH) evolving from traumatic subdual hydroma (TSH). Methods: The clinical characteristics of 44 patients with CSDH evolving from TSH were analysed retrospectively and the relevant literature was reviewed. Results: In 22.6% of patients, TSH evolved into CSDH. The time required for this evolution was 14–100 days after injury. All patients were cured with haematoma drainage. Conclusions: TSH is one possible origin of CSDH. The clinical characteristics of TSH evolving into CSDH include polarization of patient age and chronic small effusion. The injuries usually occur during deceleration and are accompanied by mild cerebral damage.

Chronic, haematoma subdural, subdural effusion, wound and injuries History Received 11 July 2013 Revised 2 October 2014 Accepted 18 November 2014 Published online 22 December 2014

Introduction

Diagnostic criteria

Traumatic subdural hydroma (TSH) is defined as the accumulation of cerebrospinal fluid (CSF) in the subdural space because of the rupture of arachnoid cysts of the brain after a head injury and was first reported by Ohno et al. [1] in 1894. Chronic subdural haematoma (CSDH) has been well-known among neurosurgeons since Li et al. [2] first described it in 1857. However, the aetiology, course, optimal care and outcome of CSDH remain unclear. With the wide application of computed tomography (CT) scanning in patients with head trauma, more patients with CSDH secondary to TSH have been identified [1–13]. The present study reports on the experience with 44 patients who developed CSDH secondary to TSH in the hospital from January 1989–June 2011.

Diagnostic criteria for TSH

Subjects and methods Sex and age A total of 44 patients were enrolled in this study, including 36 males and eight females. Their age distribution is provided in Table I. Types of head injury

The criteria for a diagnosis of TSH included [14]: (a) hydroma, especially appearing within 10 days after trauma; (b) a CT scan showing a crescent-shaped homogenous low-density area similar to CSF, with compression of the adjacent portions of the cerebrum and effacement of adjacent sulci; (c) a CT value of the lesion below 20 Hu; and (d) the membrane of the lesion is usually not enhanced. Diagnostic criteria for CSDH The criteria for a diagnosis of CSDH included [15]: (a) subdural haematoma occurring 3 weeks after head trauma; (b) a CT value of the lesion over 20 Hu; (c) a CT scan showing a crescent-shaped mixed-density or iso-density area with spaceoccupying effect and often enhancement of lesion membrane; and (d) a magnetic resonance imaging (MRI) scan showing high-signal lesions in both T1-weighted and T2-weighted images 2–3 weeks after haemorrhage or a low-signal lesion with the signal higher than that of CSF in T1-weighted images and a high-signal in T2-weighted images more than 3 weeks after bleeding.

The types of head injury are indicated in Table II. All the patients had no history of repeat head injury during the period of TSH development into CSDH.

Diagnostic criteria for CSDH evolved from TSH

Correspondence: Dr Yuguang Liu, Department of Neurosurgery, Qilu Hospital of Shandong University, and Brain Science Research Institute of Shandong University, Jinan 250012, PR China. Tel: +8613506402089. Fax: +86-531-82169114. E-mail: [email protected]

Initial CT scanning showed subdural hydroma after head trauma and repeated CT findings showed the subdural hydroma that had evolved into CSDH. The outcomes of the selected 32 patients were not retrospectively analysed and compared with the cotemporaneous cases, but rather summarized for all patients.

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Table I. Age distribution of 32 patients with TSH developing into CSDH.

Table IV. Occurrence time of TSH found by CT scan of 32 patients.

Age distribution (years)

Time after head injury (days)

No. of patients

1 month/12–10 11–20 21–30 31–40 41–50 51–60 4 61

10 2 1 3 6 4 18

51 1–3 3–7 47

No. of patients 11 21 8 4

Table V. Sites of TSH of 32 patients. Table II. Types of head injury of 32 patients.

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Types of head injury

Sites of TSH

No of patients

Traffic accidents Fall injury Hit injury Delivery injury

22 14 7 1

Table III. Symptoms and signs of CSDH in 32 patients.

Symptoms Headache Dizziness Nausea Vomiting Hypomnesia Tinnitus Diplopia

No. of patients 44 40 29 16 15 13 9

Signs dysphoria abnormal mentality obscurity papilledema hemiplegia mild aphasia positive Babinski’sign

No. of patients 5 24 11 19 22 9 18

Unilateral Frontal Fronto-temporal Fronto-parieto-temporal Parietal Bilateral Frontal One-side frontal and the other fronto- parietal

No. of patients 32 14 5 12 1 12 9 3

Table VI. Time of ‘TSH developing into CSDH. Time after head injury (days) 14–20 20–30 30–50 50–100

No. of patients 1 13 19 11

Results Incidence The incidence of the evolution of TSH into CSDH varied largely with age from 2.4–56%. In this hospital, patients with TSH accounted for 3.6% of all trauma patients during the study period and this incidence was possibly related to the severity and type of trauma. Evolution of CSDH was associated with surgery, but not the severity of the trauma. Symptoms and signs On the basis of TSH manifestations, 44 patients presented deterioration after alleviation, the reappearance of former symptoms and signs of TSH or the appearance of new symptoms and signs. The symptoms and signs of CSDH are listed in Table III. Primary symptoms at presentation differed with the severity of trauma, but all were related to primary trauma. During the development, all patients suffered from effusion-related symptoms such as contralateral muscle weakness and mental decline, especially those undergoing surgery later. However, no signs related to acute increased intracranial pressure such as cerebral hernia were reported before evolution into haematoma. CT findings Each patient underwent CT scanning at least twice. MRI scanning was performed in 32 patients also. The occurrence of TSH confirmed by CT scan is presented in Table IV and the

sites of TSH are listed in Table V. The volume of unilateral TSH ranged from 7–50 ml (mean ¼ 24 ml) and the volume of bilateral TSH varied from 25–70 ml (mean ¼ 36 ml). The CT value of hydromas ranged from 5–15 Hu. Skull fractures were found in three patients, cerebral contusions in four patients and subarachnoid haemorrhage and small epidural haematoma in one patient each. The time taken for the development of’ TSH into CSDH is shown in Table VI. CT scans showed subdural crescent space-occupying lesions in all patients with CSDH. The sites in 32 patients with unilateral haematoma were in accordance with those of the original subdural hydromas. Among them, a low-density area appeared in four cases, mixed-density in 15 cases and high-density in 13 cases on CT films. Among the 12 cases of bilateral haematomas, mixed-density areas were observed in 12 cases and highdensity areas in four cases. The CT values of the lesions ranged from 25–50 Hu. MRI scans showed high-signal lesions in both T1-weighted and T2-weighted images. Treatments All of the patients underwent unilateral or bilateral craniopuncture and drainage of CSDH under local anaesthesia. The volumes of haematomas varied from 30–150 ml (mean ¼ 65 ml). The drainage lasted for 2–3 days after operation. Other treatments were mainly aimed at the primary craniocerebral trauma, including those for the protection and nourishment of

DOI: 10.3109/02699052.2014.990513

the brain tissues and prevention of complications as well as other symptomatic treatments. During the perioperative period, cases of CSDH evolving from TSH only received conventional treatment such as proper dehydration to reduce the intracranial pressure, but no anti-platelet drugs, because no definitive evidence proved that changing platelet activity is beneficial for recovery. Previous experimental models revealed that blood breakdown products are directly related to blood accumulation. However, the method for changing the process is to change the local factors but not the blood constituents. Surgery had a definitive effect and adjuvant medication was unnecessary.

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Outcomes Post-operatively, the symptoms and signs of all patients, such as headache and hemipanalysis, were relieved or disappeared immediately. No complications or death occurred. Repeated CT scans showed that CSDH disappeared in all patients by 1–2 months after operation. All patients recovered and had no sequelae related to the haematoma. Surgery-related perioperative complications such as diabetes mellitus and cerebral thrombosis but no haematoma-related sequelae were reported. All patients were followed up for 2–24 years. No cases of recurrence occurred.

Discussion Incidence of TSH developing into CSDH Yamada et al. [11] reported three cases of TSH developing into CSDH in 1980. Afterwards, the incidence of TSH developing into CSDH was reported to vary from 9–58% in the literature [1–13]. Park et al. [9] described 13 of 145 patients with TSH developing into CSDH. Lee et al. [3] presented 69 cases of TSII and TSH with evolution into CSDH in eight cases. Koizumi et al. [8] observed 38 cases of TSH and CSDH evolved from TSH in four cases. In addition, 12 cases of CSDH originated from 24 cases of TSH reported by Yamada et al. [4]. Ohno et al. [1] reported that the incidence of TSH developing into CSDH was as high as 58%. In China, Li et al. [2] observed 39 cases of TSH and TSH transformed into CSDH in eight cases. The incidence of TSH evolution to CSDH was 13.9% (10/72) in a study by Chen and Chen [12] and 16.7% (32/192) in a previous study [15]. Pathogenesis of evolution The pathogenesis of TSE developing into CSDH cannot be explained satisfactorily by a single theory. Currently, several hypotheses have been proposed. (a) CSDH actually evolves from acute subdural haemorrhage [8, 16]. The reason is that acute subdural haemorrhage cannot be ruled out completely only on the basis of a lowdensity lesion shown by CT scan and it is misdiagnosed as TSE. Therefore, CSDH is mistaken as evolving from TSE. However, this theory cannot explain the difference between the time for acute subdural haemorrhage to change into a low-density lesion and the time for TSE to occur. Usually, TSE occurs within 1 week after trauma, whereas the transformation of acute subdural

Chronic subdural haematoma evolving from TSE

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haemorrhage images on CT scans from hyper-density to hypo-density takes more than 2 weeks [4]. (b) The subdural hydroma is the source of CSDH [3]. Persistent collection of subdural fluid may lead to the formation of a membrane and the gradually increased effusion results in the rupture of bridging-veins or cyst wall bleeding. This can also explain why TSE evolving into CDSH often happens 1 month after head injury, when the membrane of the hydroma has developed. (c) Hyperfunction of fibrinolysis in the hydroma leads to a blood coagulation disorder. As a result, CSDH comes into being as the bleeding continues. Suzuki et al. [17, 18] investigated the involvement of inflammation, coagulation and fibrinolysis in the development and propagation of CSDH by measuring the levels of inflammatory cytokines in peripheral venous blood and subdural fluid obtained from 34 patients with CSDH and from nine patients with TSE and concluded that inflammatory cytokines may be involved in the continuous development from TSE to CSDH. (d) The properties of TSE change. The protein contents or blood components are mingled in the hydroma, which results in TSE evolving into CSDH [2, 6]. (e) Repeated head trauma causes bleeding in the hydroma and evolves into CSDH [2, 13]. In the present study, clinical and imaging changes revealed that the capsule of the subdural effusions caused hyperfibrinolysis in the effusion, resulting in coagulation disorder and infiltration and accumulation of blood constituents into the effusion to form the haematoma. Surgery interrupts capsule formation around the effusion and the changes in blood constituents. Therefore, this treatment is effective. The nature of post-traumatic effusion will be further analysed to explore the relationship between the formation of a haematoma and the prognosis, which is expected to be helpful for the classification and treatment of effusions. Clinical characteristics The clinical characteristics of TSE evolving into CSDH are as follows: (a) The ages of patients are polarized. Children under 10 years old or persons over 60 years old represent the overwhelming majority of patients, which may be related to the large subdural space in children and aged people. (b) It often occurs in patients with chronic small or medium effusion who are undergoing conservative treatment. The subdural effusion can transform into a hydroma in the course of conservative treatment in patients with small or medium subdural effusions. Bleeding appears in the membrane of the hydroma during its formation, leading to CSDH. The evolution of TSH into CSDH seldom happens in cases of TSE treated surgically. The cause may be that the early operation interrupts the course of effusion development into a hydroma and the formation of a membrane. (c) The patients are often injured during deceleration. (d) The accompanying craniocerebral damage is often mild.

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Treatment and prognosis In principle, early craniopuncture and haematoma drainage should be carried out in patients with a TSH evolving into CSDH. However, conservative treatment can be performed for a patient with a small CSDH with no symptoms under the dynamic observation of a CT scan. There have been no deaths related to haematomas in patients treated surgically or conservatively according to the literature and the data [1–13, 15]. Thus, the patients with TSH developing into CSDH are thought to have a better prognosis than those with TSH.

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Future directions TSH is one of the main complications associated with brain trauma and many cases of TSH ultimately evolve into CSDH. Despite intensive studies and recent advances in surgical treatments for CSDH, the pathogenesis of TSH evolving into CSHD remains incompletely understood and the effective management of TSH evolving into CSHD has yet to be achieved. It is expected that breakthroughs in several areas may help provide a better understanding and management of the evolution of TSH into CSHD. For example, a prospective study with MRI and CT monitoring of the different stages of the evolution of TSH into CSHD is necessary to gain insight into the disease progression. The development of novel surgical procedures will be important for the successful treatment of CSHD evolved from TSH. Finally, a detailed analysis of fluids drawn intra-operatively could reveal molecular mechanisms underlying the evolution of TSH into CSHD.

Declaration of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

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3. Lee KS, Bae WK, Doh JW, Bae HG, Yun IG. Origin of chronic subdural haematoma and relation to traumatic subdural lesions. Brain Injury 1998;12:901–910. 4. Yamada H, Nihei H, Watanabe T, Shibui S, Murata S. Chronic subdural hematoma occurring consequently to the posttraumatic subdural hygroma–on the pathogenesis of the chronic subdural hematoma (author’s transl). No To Shinkei 1979;31:115–121. 5. Murata K. Chronic subdural hematoma may be preceded by persistent traumatic subdural effusion. Neurologica Medica Chirurgica (Tokyo) 1993;33:691–696. 6. Takahashi Y, Sato H, Inoue Y, Takeda S, Ohkawara S. CT findings and the evaluation of chronic subdural hematoma (Part I)–forecast of chronic subdural hematoma (author’s transl). Neurologica Medica Chirurgica (Tokyo) 1981;21:485–490. 7. Nakamura N, Ogawa T, Hashimoto T, Yuki K, Kobayashi S. Reevaluation on resolving subdural hematoma (author’s transl). Neurologica Medica Chirurgica (Tokyo) 1981;21:491–500. 8. Koizumi H, Fukamachi A, Wakao T, Tasaki T, Nagaseki Y, Yanai Y. Traumatic subdural hygromas in adults–on the possibility of development of chronic subdural hematoma (author’s transl). Neurologica Medica Chirurgica (Tokyo) 1981;21:397–406. 9. Park CK, Choi KH, Kim MC, Kang JK, Choi CR. Spontaneous evolution of posttraumatic subdural hygroma into chronic subdural haematoma. Acta Neurochirurgica (Wien) 1994;127:41–47. 10. Zhang SG, Wang WH, Xu L. The dynamic change of traumatic subdural hydroma. Clinical Journal of Neurology 1998;21: 183–184. 11. Yamada H, Watanabe T, Murata S, Shibui S, Nihei H, Kohno T, Itoh T. Developmental process of chronic subdural collections of fluid based on CT scan findings. Surgical Neurology 1980;13: 441–448. 12. Chen WF, Chen JQ. Evolution of traumatic subdural hydroma into chronic subdural hematoma – a report of 10 cases. Jiangsu Medical Journal 2000;26:398–399. 13. Wang CH, Hu JQ. Transformation of traumatic subdural hydroma into chronic subdural hematoma. Chinese Journal of Clinical Neurosurgery 2000;16:299–300. 14. St John JN, Dila C. Traumatic subdural hygroma in adults. Neurosurgery 1981;9:621–626. 15. Liu Y, Gong J, Li F, Wang H, Zhu S, Wu C. Traumatic subdural hydroma: clinical characteristics and classification. Injury 2009;40: 968–972. 16. Lee KS. Natural history of chronic subdural haematoma. Brain Injury 2004;18:351–358. 17. Suzuki M, Endo S, Inada K, Kudo A, Kitakami A, Kuroda K, Ogawa A. Inflammatory cytokines locally elevated in chronic subdural haematoma. Acta Neurochirurgica (Wien) 1998;140: 51–55. 18. Suzuki M, Kudo A, Kitakami A, Doi M, Kubo N, Kuroda K, Ogawa A. Local hypercoagulative activity precedes hyperfibrinolytic activity in the subdural space during development of chronic subdural haematoma from subdural effusion. Acta Neurochirurgica (Wien) 1998;140:261–265; discussion 5–6.

Chronic subdural haematoma evolving from traumatic subdural hydroma.

This study aimed to investigate the incidence and clinical characteristics of chronic subdural haematoma (CSDH) evolving from traumatic subdual hydrom...
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