Clinical Factors of Recurrent Chronic Subdural Hematoma

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1 Neurol Med Chir (Tokyo) 41, , 2001 Clinical Factors of Recurrent Chronic Subdural Hematoma Makoto OISHI, MakotoTOYAMA, ShinichiTAMATANI, Tomoji KITAZAWA, andmasatsunesaito Department of Neurosurgery, Nagaoka Red Cross Hospital, Nagaoka, Niigata Abstract The clinical, radiological, and operative factors of recurrent chronic subdural hematoma (CSDH) were retrospectively analyzed in 116 patients with CSDH in 134 hemispheres, treated by one burr hole surgery. The correlation of was evaluated with personal and clinical factors such as age, sex, history of head injury, and interval from onset of initial symptoms to hospitalization; laboratory findings such as bleeding tendency and liver function; computed tomography (CT) findings such as hematoma density and brain atrophy; and operative findings such as additional procedures and postoperative residual air. The group (RG) included 10 hemispheres (7.5%) in 10 patients (8.6%). The interval from onset of symptoms to hospitalization was significantly shorter in the RG than in the non group (NRG). Headache was more frequently seen in the RG than in the NRG. Density of hematoma on CT was classified into five types: Low, iso, and high density, niveau, and mixed, and the incidence of was 0%, 2.3%, 17.2%, 12.5%, and 6.5%, respectively. Larger amounts of residual air in the postoperative hematoma cavity were associated with of CSDH. CSDH that progresses rapidly in the acute stage and appears as high density on preoperative CT is associated with a high incidence of. Intraoperative air invasion to the hematoma cavity should be avoided to prevent. Key words: chronic subdural hematoma,, clinical review, computed tomography, burr hole surgery Introduction Chronic subdural hematoma (CSDH) is one of the most common diseases in neurosurgical practice. One burr hole evacuation and irrigation of the subdural hematoma with or without closed-system drainage has been widely accepted as the optimum method for treating CSDH for the last two decades. 3,4,9,10,14,18,19) The most important advantages of this method is that diagnosis requires minimal examination and that a relatively noninvasive procedure results in a satisfactory outcome even for older or high-risk patients. However, all neurosurgeons have experienced some recurrent cases of this disease after treatment with this method, with an incidence as variable as 3% to 20%. 1,2,4,8,18,20) Various aspects of recurrent CSDH, such as the patient's condition, the mechanism of growth, clinical and radiological features, and additional operative procedures have been discussed. 2,5,11,16 18,20) However, prediction of remains unattainable. This study reviewed the general and neurosurgical practices used to treat our patients with CSDH and retrospectively evaluated the clinical factors of recurrent CSDH. Materials and Methods 116 patients with CSDH (134 hemispheres) were treated surgically at our hospital between January 1995 and March Cases of infantile CSDH and subdural effusion without typical neomembrane were excluded. Recurrence of CSDH was defined as reaccumulation of the hematoma within the postoperative hematoma cavity and the reappearance of neurological symptoms. On admission, all patients underwent complete neurological examination and various detailed information, such as history of head injury, initial Received March 13, 2001; Accepted June 27, 2001 Author's present address: M. Oishi, M.D., Department of Neurosurgery, National Nishi-Niigata Chuo Hospital, Niigata, Japan. 382

2 Clinical Factors of Recurrent CSDH 383 symptoms and date they appeared, alcohol abuse, and receipt anticoagulant or antiplatelet therapy, was collected from the patient or family members. Few preoperative laboratory studies were performed but included bleeding time, platelet counts, and activated partial thromboplastin time to assess hemostatic function, and glutamine-oxaloacetic transaminase, glutamic-pyruvic transaminase, gamma guanosine triphosphate (ggtp), and lactate dehydrogenase (LDH) analysis to assess liver function. The diagnosis of CSDH was confirmed by computed tomography (CT) obtained on the day of admission in all patients. The presence of uni- or bilateral hematoma, hematoma density, and brain atrophy were evaluated. Hematoma density was classified into five types: Low, iso, and high density relative to the brain, niveau, and mixed. Brain atrophy was classified into three stages: No or mild atrophy, definite atrophy such as dilated sulci, and severe atrophy such as widely dilated sulci and subdural space. One burr hole surgery under local anesthesia was performed in all hemispheres. Two surgical procedures were used for evacuating the hematoma after one burr hole craniotomy and opening the dura mater. In one method, the hematoma was evacuated after cutting the outer membrane, the cavity was irrigated repeatedly with natural saline, and a closedsystem drainage tube was inserted in the cavity. In the other method, no evacuation and irrigation of the hematoma was performed, as the closed-system drainage tube was inserted into the hematoma cavity immediately after cutting the outer membrane, and the skin was closed. Thedrainagetubewasusuallyleftinplacefor1or 2 days after the operation. The volume of the hematoma was measured. CT was performed on the first day after the operation, and the level of residual air invading the subdural cavity was classified into three stages: No or mild residual air bubbles, definite residual air, and severe residual air such as almost total replacement with air. All patients were followedupfor3ormoremonthsuntilthediseasewas regarded as in remission. Results CSDH recurred in 10 hemispheres (7.5%) of 10 patients (8.6%). Reoperation was performed in nine patients, and one patient with obvious reaccumulation of the hematoma and reappearance of mild symptoms was observed over the long term and slowly improved. The difference in the incidence of CSDH in the eight men (9.5%) and two women (6.3%) was not significant. Mean age (±1 Table 1 Characteristics and clinical findings in the group (RG) and the non group (NRG) RG NRG Total (n = 10) (n = 106) (n = 116) Sex male 8 [9.5] 76 [90.5] 84 (72.4) female 2 [6.3] 30 [93.8] 32 (27.6) Mean age (yrs) 74.2 ± ± ± 11.4 Alcohol abuse 3 (30) 11 (10.4) 14 (12.1) Anticoagulant or antiplatelet 0 (0) 11 (10.4) 11 (9.5) History of head injury 3 (30)* 77 (72.6) 100 (86.2) Days from appearance of symptoms 4.9 ± 4.7* 9.5 ± ± 9.8 Preoperative symptoms headache 5 (50) 28 (26.4) 33 (28.4) psychomotor disturbance 3 (30) 48 (45.3) 51 (44.0) hemisyndrome 6 (60) 64 (60.4) 70 (60.3) Age and days from appearance of symptoms are mean ± SD. *Significantly different from NRG (pº0.05). [ ]: percentage of cases in males or females, ( ): percentage of cases in each group. SD) of patients in the group (RG) (74.2 ± 7.8 years) was not significantly different from that in the non group (NRG) (70.8 ± 11.7 years). Patients in the RG tended to have a history of alcohol abuse (30%) compared with the patients in the NRG (10.4%), but the difference was not significant. No of CSDH was found in patients receiving anticoagulation or antiplatelet therapy (Table 1). The incidence of head injury in the RG was significantly lower than that in the NRG, and the interval from the onset of first symptoms to hospitalization was significantly shorter in the RG than that in the NRG (Table 1). Hemisyndromes, psychomotor disturbances, and headache were common as preoperative symptoms (Table 1). Five of 10 patients (50%) in the RG complained of headache, compared with 28 of 106 patients (26.4%) in the NRG, but there was no significant difference in this small group. Preoperative laboratory studies found ggtp level in the RG was over the normal limit, and in the NRG was within the normal limit, but this difference was not significant. LDH levels in both groups were over the normal limit, but there were no significant differences between the groups. All other results were within normal limits, and there were no significant differences between the two groups (Table 2). One of the 18 patients (5.6%) with bilateral CSDHs experienced in only one side, and was not significantly different from the nine of 98 patients (9.2%) with unilateral CSDH. The relationship between the density of hematoma on CT and

3 384 M. Oishi et al. Table 2 Laboratory findings in the group (RG) and the non group (NRG) Parameters Normal range RG NRG Platelets ( 10 4 /mm 3 ) ± ± 8.4 Bleeding time (min) ± ± 1.3 APTT (sec) ± ± 5.3 GOT (IU/l) ± ± 11 GPT (IU/l) ± ± 9 ggtp (IU/l) ± ± 60 LDH (IU/l) ± ± 135 Data are mean ± SD. APTT: activated partial thromboplastin time, ggtp: gamma guanosine triphosphate, LDH: lactate dehydrogenase, GOT: glutamine-oxaloacetic transaminase, GPT: glutamicpyruvic transaminase. Table 3 Hematoma density Hematoma density on computed tomography and incidence of hemispheres Low (n = 15) 0 0% Iso (n = 43) 1 2.3% High (n = 29) % Niveau (n = 16) % Mixed (n = 31) 2 6.5% Table 4 Brain atrophy and incidence of Brain atrophy cases No or mild atrophy (n = 64) 6 9.4% Definite atrophy (n = 35) 2 5.7% Severe atrophy (n = 17) % Table 5 Amount of residual air Postoperative residual air in the subdural cavity and incidence of hemispheres None or mild (n = 83) 2 2.4% Definite (n = 37) % Severe (n = 14) % the incidence of is shown in Table 3. The incidence of in the high-density group (17.2%) was higher than that in any other group, but was not significant. There was no correlation between the incidence of and severity of brain atrophy (Table 4). Evacuation and irrigation of the hematoma followed by drainage was performed in 117 hemispheres but only drainage in the other 17 hemispheres. Recurrence was observed in eight sides (6.8%) treated by evacuation and irrigation procedure and two sides (11.8%) treated by only drainage, with no significant difference. The volume of evacuated or drained hematoma in the RG (134.9 ± 50.8 cm 3 ) was greater than that in the NRG (109.4 ± 44.6 cm 3 ), but the difference was not significant. The incidence of was higher with greater amounts of residual air on postoperative CT (Table 5). Severe residual air was found in 14 of 117 sides (12.0%) treated by the evacuation and irrigation procedure, but no sides treated by only drainage. Discussion Risk factors for the of CSDH are generally divided into three categories: Factors associated with patient characteristics, such as age, sex, alcohol abuse, bleeding tendency, brain atrophy, or intracranial hypotension; factors associated with the pathogenesis of CSDH, such as the structure of the neomembrane or the characteristics of the hematoma; and factors associated with surgery, such as timing or additional procedures of irrigation or closedsystem drainage. Age, bleeding tendency, brain atrophy, alcohol abuse, and bilateral CSDHs have been reported as risk factors for. 2,5,9,20) However, the present study did not confirm these factors as risks. The incidence of head injury in the RG was significantly lower in our present series, but this could be a misleading finding. Injuries capable of causing CSDH could be so mild that the patients did not notice or remember the incident later. Previously, a higher incidence of head injury was found in recurrent cases. 2,20) CSDH progressed more rapidly in the period from onset of leading symptoms to hospitalization in the RG than in the NRG. Headache, which indicates rapid CSDH growth causing increasing intracranial pressure, was also a frequent preoperative symptom in the RG. Patients with high-density CT areas had the largest incidence of. The density of the CSDH is considered to indicate the age of the lesion, and high density is generally considered to indicate that the hematoma involves much fresh bleeding. 2,15) Niveau consisted of a lowor iso-density upper layer and a high-density lower layer, so could be considered as closely related to the high-density category. Classification of the hematomas into two groups combining the high-

4 Clinical Factors of Recurrent CSDH 385 density and niveau groups, and the low- and isodensity groups showed that the incidence of CSDH in the former group (15.6%) was significantly higher than that in the latter group (1.7%). These results indicate that CSDH with rapid progression in the relatively acute phase and appearing as high density on CT have a high incidence of. Similar hypotheses for the mechanism of CSDH growth have been developed based on pathological investigations. 7,9,17) Inflammatory reaction in the dural inner membrane evoked by blood in the subdural space leads to the formation of the neomembrane, and the outer membrane of this neomembrane has rich capillaries that repeatedly follow a cycle of microbleeding and fibrinolysis, which contributes to CSDH growth. This pathogeneticbased hypothesis suggests that the neomembrane in recurrent cases is vulnerable and susceptible to repeat microbleeding into the hematoma cavity over the short term, and could explain the high density on CT in our recurrent cases. Consequently, our results strongly support this mechanism of. Similar results were reported from clinical findings and CT findings of recurrent cases. 2) However, review of preoperative CT and magnetic resonance (MR) imaging of CSDH in 230 patients found no relationship between rate and CT findings, and that only T 1 -weighted MR images were useful in predicting. 18) Possibly, there is another mechanism of. We consider burr hole surgery to be the best method as initial treatment for this disease because it is relatively noninvasive and applicable to older or high-risk patients although the validity and safety of craniectomy are known. 6) Our results also show that postoperative residual air in the subdural cavity increases the incidence of. Persistence of the postoperative subdural cavity is a risk factor for reaccumulation of the hematoma, 5,10,13,14) and the presence of postoperative residual air is believed to prevent reduction of the cavity. 2,12) Therefore, efforts to prevent air from entering the hematoma cavity intraoperatively may be important. Our results could not definitely conclude whether irrigation of a hematoma is really necessary, but possibly irrigation should be avoided to prevent complications due to sudden decreases in intracranial pressure and intraoperative air invasion. 16) Actually, all sides with severe residual air had undergone the irrigation procedure. In the present study, no factors associated with patient characteristics were confirmed as risks for recurrent CSDH, but some factors associated with the pathogenesis of CSDH and surgery were risks for. Based on the pathogenesis of CSDH, we conclude that the timing of surgery is important and that CSDH with rapid progression in the relatively acute phase and appearing as high density on CT is prone to recur because of the vulnerability of the capillaries of the neomembrane. Therefore, the operation should be delayed unless severe symptoms are present, and undertaken at a later stage when the CSDH appears as iso or low density on CT. For the operativeprocedure,oneburrholesurgeryisthe best method for treating CSDH, but avoiding intraoperative air invasion is also important to prevent. References 1) Arbit E, Patterson RH Jr, Fraser RAR: An implantable subdural drain for treatment of chronic subdural hematoma. Surg Neurol 15: , ) Asano Y, Hasuo M, Takahashi I, Shimosawa S: [Recurrent cases of chronic subdural hematoma: its clinical review and serial CT findings]. No To Shinkei 44: , 1992 (Jpn, with Eng abstract) 3) Camel M, Grubb RL Jr: Treatment of chronic subdural hematoma by twist-drill craniostomy with continuous catheter drainage. J Neurosurg 65: , ) Ernestus RI, Beldzinski P, Lanfermann H, Klug N: Chronic subdural hematoma: surgical treatment and outcome in 104 patients. Surg Neurol 48: , ) Fukuhara T, Gotoh M, Asari S, Ohmoto T, Akioka T: The relationship between brain surface elastance and brain reexpansion after evacuation of chronic subdural hematoma. Surg Neurol 45: , ) Hamilton MG, Frizzell JB, Tranmer BI: Chronic subdural hematoma: The role for craniotomy reevaluated. Neurosurgery 33: 67 72, ) Ito H, Komai T, Yamamoto S: Fibrinolytic enzyme in the lining walls of chronic subdural hematoma. JNeurosurg 48: , ) Laumer R, Schramm J, Leykauf K: Implantation of a reservoir for recurrent subdural hematoma drainage. Neurosurgery 25: , ) Markwalder TM: Chronic subdural hematomas: a review. J Neurosurg 54: , ) Markwalder TM, Steinsiepe KF, Rohner M, Reichenbach W, Markwalder H: The course of chronic subdural hematoma after burr-hole craniostomy and closed-system drainage. JNeurosurg55: , ) Nagata K, Asano T, Basugi N, Tango T, Takakura K: [Studies on the factors affecting the reduction of chronic subdural hematoma: effect of preoperative factors with special reference to cerebral atrophy]. No Shinkei Geka 16: , 1988 (Jpn, with Eng abstract) 12) Nagata K, Asano T, Basugi N, Tango T, Takakura K: [Studies on the operative factors affecting the reduc-

5 386 M. Oishi et al. tion of chronic subdural hematoma, with special reference to the residual air in the hematoma cavity]. No Shinkei Geka 17: 15 20, 1989 (Jpn, with Eng abstract) 13) Oku Y, Takimoto N, Yamamoto K, Onishi T: Trial of a new operative method for recurrent chronic subdural hematoma. JNeurosurg61: , ) Robinson RG: Chronic subdural hematoma: surgical management in 133 patients. J Neurosurg 61: , ) Scotti G, Terbrugge K, Melancon D, Belanger G: Evaluation of the age of subdural hematomas by computerized tomography. J Neurosurg 47: , ) Suzuki K, Sugita K, Akai T, Takahata T, Sonobe M, Takahashi S: Treatment of chronic subdural hematoma by closed-system drainage without irrigation. Surg Neurol 50: , ) Takahashi Y, Ohkura A, Yoshimura F, Ochiai S, Hirohata M, Shigemori M: Ultrastructure of collagen fibers in the outer membrane of recurrent chronic subdural hematoma. Neurol Med Chir (Tokyo) 36: , ) Tsutsumi K, Maeda K, Iijima A, Usui M, Okada Y, Kirino T: The relationship of preoperative magnetic resonance imaging findings and closed system drainage in the of chronic subdural hematoma. J Neurosurg 87: , ) Wakai S, Hashimoto K, Watanabe N, Inoh S, Ochiai C, Nagai M: Efficacy of closed-system drainage in treating chronic subdural hematoma: a prospective comparative study. Neurosurgery 26: , ) Yoshii K, Seki Y, Aiba T: [Causative factors of of chronic subdural hematoma]. No Shinkei Geka 15: , 1987 (Jpn, with Eng abstract) Address reprint requests to: M.Oishi,M.D.,Departmentof Neurosurgery, Brain Research Institute of Niigata University, Asahimachi dori, Niigata , Japan. Commentary Clinical factors causing reaccumulation of chronic subdural hematoma may be categorized into the patient's condition and the surgical methods. The former includes the amount of free space due to brain atrophy, blood coagulability, the rate of accumulation speed, etc. The surgical method varies in each hospital but can be roughly classified into open drainage with irrigation and closed drainage. In this paper, the authors pointed out two factors causing reaccumulation of the hematoma: density of hematoma on CT and accumulation of subdural air after surgery. The former may indicate that the closed drainage system might reduce the risk of postoperative air accumulation, but was less effective for irrigation of fresh hematoma showing high intensity on CT. The authors conclude as well that the volume of subdural free space by brain atrophy or blood coagulability was not influential on reaccumulation of the hematoma, but should statistically be evaluated again with a larger number of the patients. Takeshi KAWASE, M.D. Department of Neurosurgery School of Medicine Keio University Tokyo, Japan