Impact of factors predisposing young patients to the development of intracranial chronic subdural haematoma

Chris Schulz^a, Cornelia Walther^a, Carsten Hackenbroch^b, Uwe Max Mauer^a, René Mathieu^a

^a Department of Neurosurgery, Bundeswehr Hospital of Ulm, Ulm, Germany

^b Department of Radiology and Neuroradiology, Bundeswehr Hospital of Ulm, Ulm, Germany

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Summary

Background. Chronic subdural haematoma (CSDH) commonly occurs after traumatic brain injury (TBI). Although elderly patients with mild TBI are most often affected, young patients too can develop CSDH in rare cases. We present three cases and describe special anatomical and demographic factors in a group of young patients with CSDH.

Methods. We conducted a retrospective analysis that included 60 patients with CSDH (< 50years of age) in order to explore the presence of predisposing factors (disorder of haemostasis, cerebrospinal fluid imbalance, cerebral malformation, drug/alcohol abuse). At least one of these predisposing factors was detected in 36 patients. We assessed the following parameters in patients with and without predisposing factors: TBI severity, time interval from TBI to diagnosis, duration of signs and symptoms, and main clinical signs and symptoms. In addition, we analysed haematoma size, recurrence and laterality, and the number of revision procedures.

Results. Headache was the most common clinical symptom, regardless of the presence or absence of a predisposing factor. The most common predisposing factors were cerebrospinal fluid hypotension (n = 13), disorders of haemostasis (n = 12), and anatomical malformations (n = 9). Patients with predisposing factors showed significantly less severe TBIs and significantly larger haematomas than patients without predisposing factors. In addition, the rates of bilateral and recurrent haematomas were higher in the group of patients with predisposing factors.

Discussion and conclusions. Young patients too can develop CSDH. Our results demonstrated some differences between patients with and patients without predisposing factors. If CSDH is detected in patients under 50 years of age, an investigation into the underlying causes and specific predisposing factors is recommended. In young patients with known predisposing factors, even trivial TBI must be thoroughly examined and patients must be made aware of the increased risk of delayed CSDH. The presence of factors predisposing to CSDH must be considered in medical tests used in deciding fitness for certain military duties.

Key words: chronic subdural haematoma, traumatic brain injury, subdural haematoma, fitness for military duties

Background

Subdural haematoma (SDH) can develop at different time points after traumatic brain injury (TBI). It is a type of bleeding that occurs between the dura mater and the arachnoid. SDHs are classified, for example, depending on the time of their onset after TBI. Acute SDHs develop over minutes to hours. Subacute SDHs appear within a few days of an injury. Subdural fluid collections that occur more than ten days after TBI are referred to as chronic subdural haematomas (CSDHs).

Chronic subdural haematoma

Pathophysiology

Inflammatory and fibrinolytic processes are suspected to be the reason why acute and subacute SDHs become chronic. A pseudomembrane forms around the haematoma, which continuously liquefies within this capsule. In many cases, the haematoma gradually enlarges (probably as a result of fluid that is drawn into the subdural space through osmosis and recurrent microbleeds from pathological vessels in the haematoma capsule [5]).

Prevalence/incidence

CSDHs are most commonly encountered in infants and the elderly (> 65 years of age) with an incidence of approximately 5 per 100,000 population per year. [12][17] Neurological signs and symptoms appear approximately 2–8 weeks after TBI. The underlying TBI is described as trivial in many cases and a history of trauma can be elicited in less than 50 % of cases. [6]

Diagnosis and treatment

Computed tomography (CT) or magnetic resonance imaging (MRI) of the head usually detect subdural haematomas rapidly and safely. Small and asymptomatic haematomas can be managed conservatively. Indications for surgery are neurological deficits secondary to the haematoma and major bleeding with relevant mass effect (e.g. a width exceeding the thickness of the calvaria on axial images [10]).

The surgical procedure of choice is burr-hole drainage (usually under local anaesthesia) and the optional placement of a subdural drain for a few days following surgery. [9] Mortality after surgery ranges from 0.5 % to 8 %, depending on patient age, concomitant diseases and treatment. [17][24] Tranexamic acid can possibly reduce the rate of CSDH recurrence, which normally is approximately 15–25 %; evidence from the literature, however, is inconclusive. [11][23] Middle meningeal artery embolisation may also be an option in the management of recurrent CSDH. [3]

Rare cases of CSDH in young patients

The formation of haematoma in elderly patients is commonly associated with cerebral atrophy, which leads to a decrease in the pressure in the subdural spaces (especially in an upright position) and thus promotes bleeding. In rare cases, however, CSDH is also seen in young adults without cerebral atrophy. [4]

As a result of its low incidence and atypical presentation, CSDH in patients under 50 years of age presents a particular problem, and a high rate of misdiagnosis is well documented in small case series. [6][13][14][15] Multiple authors have reported a number of factors predisposing young adults to the development of CSDH (e.g. impaired haemostasis, imbalance in CSF dynamics/pressure, cerebral or cerebrovascular malformations, and chronic drug and alcohol abuse). [2][12][14][16][22] Not all young patients with CSDH, however, show such risk factors. Whether or not there are differences in patient histories, clinical and imaging findings, and postoperative courses (depending on the presence or absence of predisposing factors) is still unclear. Possible differences and their consequences are described in this article.

Case presentations

Case 1: CSDH in a patient with platelet function inhibition

A 21-year-old male soldier was taking high-dose aspirin and ibuprofen for one week following dental treatment. During a military ceremony, he experienced an episode of syncope. He fell and hit the back of his head but did not appear to have sustained any major injury. Over the following days, the patient suffered not only from ongoing dental pain but also from headaches that increased despite his self-medicating with the aforementioned combination of analgesics. Approximately two weeks after the fall, he also experienced a tingling sensation (paraesthesia) in his right arm and on the right side of his face. On account of these symptoms, he presented to a military physician who referred the patient to the Department of Neurology at the Bundeswehr Hospital of Ulm. Unenhanced computed tomography (CT) of the head was performed immediately and demonstrated a left-sided frontotemporal CSDH (Fig. 1A). The patient had no memory of a relevant TBI. Preoperative diagnostic tests for assessing coagulation showed a suppression of platelet function consistent with the prolonged use of acetylsalicylic acid.

Burr-hole surgery was performed under local anaesthesia and the haematoma was completely drained (Fig. 1B). The patient fully recovered within a few days.

Figure 1 (Case 1): Before surgery, unenhanced computed tomography (CT) of the head demonstrated a left-sided frontotemporal CSDH (red arrows) with a midline shift to the right (A). After burr-hole surgery, the haematoma was completely drained and the cerebral falx is seen again at the midline (B).

Case 2: CSDH in a patient with a temporal arachnoid cyst

A 43-year-old male patient with right-sided hemiparesis, aphasia, and decreased consciousness was admitted to the emergency department of the Bundeswehr Hospital of Ulm with a suspected diagnosis of cerebral ischaemia. A CT of the head demonstrated a large left-sided chronic subdural haematoma that caused the signs and symptoms (Fig. 2A). Neither a physical examination nor CT suggested a history of a significant head injury. Diagnostic blood coagulation tests, including platelet function tests, were normal.

Burr-hole surgery was performed under local anaesthesia and the haematoma was removed. Imaging demonstrated decompression of the left cerebral hemisphere (Fig. 2B). The patient’s neurological signs and symptoms rapidly resolved. The patient had no memory of a relevant TBI. For this reason, a large arachnoid cyst that was detected by magnetic resonance imaging (MRI) in the region of the left temporal pole was assumed to be the cause of CSDH (Fig. 2C).

Figure 2 (Case 2): CT of the head demonstrated a large left-sided chronic subdural haematoma and a massive shift of brain tissue to the right (A). After burr-hole surgery, marked decompression of the left cerebral hemisphere can be seen (B). MRI detected a large arachnoid cyst in the region of the left temporal pole (C).

Case 3: CSDH after epidural anaesthesia

A 22-year-old refugee from Syria who was pregnant for the fourth time presented to a maternity hospital to give birth at full term. She had had three uncomplicated spontaneous deliveries in her homeland and an uneventful fourth pregnancy. The patient had a spontaneous delivery under epidural anaesthesia (which was documented to have led to a CSF leak). The delivery was described as normal.

The mother and her child had been staying on the maternity ward for three days when the young woman suddenly experienced severe positional headaches. The patient underwent diagnostic CT for suspected cerebral venous sinus thrombosis. CT, however, did not detect any abnormal findings and, above all, did not show any signs of intracranial vascular thrombosis (Fig. 3A). On the following days, the patient’s headaches worsened and were treated with symptomatic medications.

Prior to discharge, the patient underwent MRI since her symptoms had not sufficiently improved. Again, imaging provided no evidence of venous thrombosis but demonstrated a small subdural haematoma (Fig. 3B), which was left untreated. Eight days after giving birth, the woman was allowed to return to her refugee accommodation.

Seven days after her discharge from hospital, she was found in a deep coma at the accommodation site and her left eye was dilated. She was immediately taken to the emergency department of the Bundeswehr Hospital of Ulm. A CT of the head demonstrated a large space-occupying CSDH (Fig. 3C), which was immediately drained surgically. Coagulation results were normal. Although the haematoma had been completely removed in an uncomplicated surgical procedure, the patient’s state of consciousness did not improve after surgery. Postoperative MRI showed that the patient’s condition was caused by extensive infarction in the left hemisphere (Fig. 3D) in the absence of vascular occlusion. For this reason, it was assumed that the patient had developed brain herniation and infarction, which led to infarct swelling a few days later (Fig. 3E). Decompressive craniectomy was proposed as a last resort but was rejected categorically by the patient’s family. The young woman died in vegetative state approximately five weeks after the birth of her fourth child.

Figure 3 (Case 3): On day 3 after delivery, unenhanced CT did not show any signs of intracranial vascular thrombosis (A). Prior to discharge from the maternity hospital (on day 8 after delivery), MRI was performed and demonstrated a small subdural haematoma, which was left untreated (B). One week later, the patient was admitted to the Bundeswehr Hospital of Ulm. A CT of the head was performed and demonstrated a large CSDH in the left cerebral hemisphere (C). After surgery, MRI showed extensive infarction involving the left hemisphere and parts of the right hemisphere (D). A few days later, CT demonstrated marked infarct swelling (E).

The role of CSDH in military medicine

From the military medical perspective, CSDH is interesting in two respects. First, young people too can obviously develop chronic haematoma after TBI which must be detected at an early stage so that spontaneous resorption can be achieved with conservative management and surgery is not required. Second, the presence of a factor predisposing to CSDH may be a reason for excluding military personnel from certain military duties where training or service are associated with an increased likelihood of trauma that may only be trivial but which can (more) easily lead to the development of intracranial haematoma in these young adults (e.g. impact trauma in combat situations, activities involving acceleration and deceleration such as flying duties or parachute jumping).

The objective of this retrospective study was to identify factors that may predispose young patients to the development of CSDH.

Methods

Patient population

From January 2000 to June 2017, a total of 526 patients with CSDH underwent surgical treatment at the Bundeswehr Hospital in Ulm. Among them were 60 patients who were younger than 50 years of age. These cases were retrospectively reviewed for the presence of predisposing factors (disorder of haemostasis, cerebrospinal fluid imbalance, cerebral malformation, drug/alcohol abuse).

Thirty-six patients showed at least one of these predisposing factors (Group A). Twenty-four patients had no predisposing factor (Group B).

Parameters

The following parameters were analysed for the two groups:

• Severity of the underlying TBI (according to the current guidelines of the German Society for Neurosurgery on the basis of the three GCS¹ categories²),
• Time interval from TBI to diagnosis,
• Duration of signs and symptoms, and
• Main clinical signs and symptoms

In addition, we also analysed available CT and MRI scans as well as operative reports and other medical records in order to obtain information on the size, laterality and recurrence of haematoma and on the number of revision procedures after treatment.

Data analysis

Demographic data as well as clinical and radiological results were examined using univariate descriptive analysis. Means and medians were provided as measures of central tendency, and minimum and maximum values and standard deviations (SD) as measures of dispersion. In addition, interval data were tested for normal distribution. All grouped data were analysed using inferential statistics for testing the hypothesis of difference.

Non-parametric tests were performed on discrete, at least ordinal data (for which a normal distribution cannot be assumed). The Mann-Whitney U test for independent samples was used to compare two groups. Pearson’s chi-squared test, Fisher’s exact test, and Kendall’s tau test were used for nominal variables. In addition, correlation tests were performed. The level of significance was set at p < 0.05 for all tests. Data were analysed using SPSS Statistics 21 (IBM).

Limitations

As a result of the retrospective nature of this study (based on given group sizes), a conventional a priori sample size calculation could not be performed. We therefore undertook a post-hoc calculation in order to assess whether the observed differences were not below a specific effect size threshold at a probability of a Type I error (alpha) of 0.05, a minimum power (1-beta, probability of a Type II error) of 0.8 and a given sample size. Calculations were performed using G*Power software (version 3.1.9.2; http://www.gpower.hhu.de). The study was approved by the ethics committee of the University of Ulm.

Results

Description of the patient population

The ratio between females and males was 20:40. The patients had a mean age of 34.5 years (median 36, minimum 5, maximum 50, SD 11.26). Fifteen patients did not remember any trauma (TBI Grade: 0). Twenty-one patients had a mild TBI (Grade 1, GCS score: 13–15). There were 17 patients with a moderate TBI (Grade 2, GCS 9–12), and 7 patients with a severe TBI (Grade 3, GCS 3–8).

Time interval from trauma to surgery

The time interval from TBI to surgical decompression was only assessable in patients who remembered their TBI (n = 45). It ranged from a minimum period of 1 week to a maximum period of 16 weeks (mean 6.53, median 6, SD 6.2). Since two patients were intubated at admission, it was impossible to determine the time period from the onset of clinical symptoms to the diagnosis of CSDH in these cases. Accordingly, this parameter was assessed in 58 patients. The period from symptom onset to diagnosis ranged from a minimum of 1 day to a maximum of 84 days (mean 17.68, median 7, SD 32.4). Diagnosis was not made until four weeks after the onset of symptoms in more than two thirds of the cases and in two cases it took as long as more than eight weeks after the initial onset of symptoms.

Clinical manifestation

Signs and symptoms

Patients presented with a wide variety of clinical signs and symptoms (Table 1). Fifteen different signs and symptoms were reported. In the majority of cases, patients had a combination of symptoms. Two patients had been intubated in the prehospital setting and were therefore unable to describe their previous subjective symptoms. Headache was the most common symptom, presenting in 52 of 58 patients.

Table 1. Frequency of clinical signs and symptoms (n = 58)

Haematoma size

Mean haematoma thickness was 1.7 cm (median 2, minimum 1, maximum 5, SD 0.89). Haematomas were found to be bilateral in 23 of the 60 patients. Fifteen patients presented with a unilateral right-sided haematoma and 22 patients with a unilateral left-sided haematoma.

Recurrences

Ten patients experienced haematoma recurrence. Haematomas recurred in 4 cases within the first week of initial surgery, in a further 4 cases after one week to one month of surgery. Recurrence occurred more than one month after surgery in only two patients: after seven weeks in one case and after five months in the other. Seven of ten patients had a single recurrence, one patient had two, and two patients had three recurrences.

Predisposing factors

Thirty-six of 60 patients had at least one predisposing factor for haematoma (see Table 2 for the frequency of factors).

Table 2. Frequency of predisposing factors related to haematoma characteristics in the group of patients with predisposing factors (n = 36)

Analysis of dependence: Group A with and Group B without predisposing factors

Age

The mean age was 36 years in Group A (median 38, minimum 9, maximum 50, SD 9.83) and 32.29 years in Group B (median 28, minimum 5, maximum 50, SD 13.6). There was no significant difference (p = 0.202, Mann-Whitney U test). Since the ratio between females and males was 1:2 in both groups, no significant difference between the groups was found (p = 1.0, Pearson’s chi-squared test).

Severity of TBI

All patients who had no memory of a TBI were in Group A. The percentage of cases with mild TBI (Grades 0 and 1, 83.3 %) was higher in Group A than in Group B (25 %, 6 of 24 cases). By contrast, the percentage of patients with a Grade 2 or Grade 3 TBI was higher in Group B (75 %).

The difference between the two groups in TBI severity was significant (p < 0.001, Pearson’s chi-squared test). In addition, there was a significant correlation between TBI severity and groups (p < 0.001, Pearson’s chi-squared test). The mean time from the onset of symptoms to diagnosis was 20.3 days in Group A (median 8.75, minimum 3, maximum 54, SD 4.9) and 13.1 days in Group B (median 7, minimum 1, maximum 42, SD 4.1). There was no significant difference (p = 0.147, Mann-Whitney U test) and no significant correlation (p > 0.1, Pearson’s chi-squared test) between the two groups in this regard. The two patients who had been intubated in the prehospital setting were in Group B.

Signs and symptoms

Headache was the most common presenting symptom in both groups and was reported by 83.3 % of the patients in Group A and by 91.7 % in Group B. There was no significant difference (p > 0.1, Pearson’s chi-squared test) and no significant correlation (p > 0.25, Pearson’s chi-squared test) between the groups in the frequency of the various clinical signs and symptoms.

Time from TBI to treatment

The time interval from TBI to treatment was longer in Group A (mean 7.33 weeks, median 8.5, minimum 3, maximum 12, SD 3.6) than in Group B (mean 5.83 weeks, median 5, minimum 1, maximum 9, SD 3.8). Half of the patients in Group A underwent treatment no earlier than four to eight weeks after trauma. By contrast, half of the patients in Group B received treatment less than four weeks after injury.

In spite of this clear trend towards earlier treatment in Group B, there was no significant difference (p = 0.208, Mann-Whitney U test) and no significant correlation (p > 0.25, Pearson’s chi-squared test) between the groups.

Haematoma size

Haematomas in Group A (with a mean thickness of 2 cm) were larger than in Group B (with a mean thickness of 1.2 cm). Group A included all haematomas with a thickness of more than 4 cm. Almost all CSDHs in Group B (23 of 24 haematomas) were smaller than 2 cm. The difference between the groups in haematoma size was significant (p < 0.001, Mann-Whitney U test). There was also a significant correlation between haematoma thickness and groups (p < 0.01, Pearson’s chi-squared test).

Laterality

Haematoma laterality was identical in both groups. Bilateral haematomas were seen in 44.4 % of the patients in Group A and in only 29.2 % of the patients in Group B. There was no significant difference (p = 0.285, Fisher’s exact test) and no significant correlation (p > 0.25, Pearson’s chi-squared test) between the groups.

Recurrence rates

The rate of recurrence was higher in Group A (22.2 %) than in Group B (8.3 %). All patients with more than one recurrence were in Group A. There was, however, no significant difference (p = 0.289; Fisher’s exact test) and no significant correlation (p > 0.1; Pearson’s chi-squared test) between the groups.

Discussion

All in all, the results of this study show that predisposing factors have a notable influence on the development of CSDH in patients under 50 years of age. A comparison of our findings with the existing literature reveals a number of points that will be discussed here in detail. It should be noted that significance tests must be considered with caution in the analyses of dependence since retrospective power analysis demonstrated that some tests were slightly underpowered. Statistical power, however, was never lower than 0.65.

Demographic and medical history factors

Sex

The ratio between males and females was 2:1 in the total patient population. This result is consistent with other studies and was observed across age group. [7][8][21] It may be attributable to the males’ generally greater accident risk.

There was also no difference between the groups of patients with and without predisposing factors in terms of the ratio between females and males. In our study, sex ratio differences were found only in the subgroups of patients with predisposing factors.

Arachnoid cysts were more commonly encountered in men. This result is in line with data reported by Zuckerman et al. [26] Likewise, the patients in the subgroup that was characterised by an “increased consumption of alcohol” were predominantly male. A likely explanation for this finding is the generally higher prevalence of alcohol dependence and abuse among men. [19]

TBI history

In our study, 75 % of all patients remembered a TBI. This percentage is comparable to that reported in similar studies. [1][7][15] In the group of patients with predisposing factors (Group A), mild TBI was more often the cause of CSDH than in the group of patients without predisposing factors (Group B). In Group A, 42 % of the patients had no memory of a TBI and a further 42 % had sustained only a mild TBI (cumulative percentage 84 %, TBI Grades 0 and 1). These findings also apply to CSDH in elderly patients. By contrast, the majority of patients in Group B, who probably developed CSDH solely as a result of their TBI, had suffered a moderate or severe TBI (cumulative percentage 75 %, TBI Grades 2 and 3). Since all patients in Group B remembered at least a mild injury, it was possible to determine the exact time of injury in all cases. A mild, moderate or severe TBI was thus required to cause CSDH in approximately 75 % of the total population of patients with CSDH. Accordingly, 25 % of all patients with a CSDH had no memory of a TBI. All these patients, however, had at least one predisposing factor. This suggests that people without a predisposing factor and without a noticeable TBI do not develop CSDH. To our knowledge, this finding, which is supported by our data, has not yet been reported in such an explicit manner. The results reported by Yang and Hunang in an article from 2017 too suggested this correlation. CSDH always has a cause, it does not arise spontaneously. A TBI (however mild it may be) or a predisposing or causative factor can always be detected. [25]

Clinical manifestation

Although no significant differences were observed between the groups of patients with and without predisposing factors in terms of specific clinical signs and symptoms, the clinical manifestation of CSDH in young patients is different from that in elderly patients. In our study, headache was the most common presenting symptom and was reported by 86.7 % of the patients. This finding is largely consistent with results reported in other studies. [13][15] The percentage of patients under 50 years of age who experienced nausea and/or vomiting was 13.3 %. In an article by Missori et al., 8.43 % of the patients aged between 20 and 50 years experienced signs and symptoms of intracranial hypertension. [15] Other studies reported similar results and found that the most common presenting signs and symptoms were headache, nausea and vomiting (i.e. typical symptoms associated with intracranial pressure) in young patients, and disturbance of consciousness, hemiparesis and mental disorders (i.e. higher cognitive dysfunctions) in elderly patients (as a result of atrophy, which can compensate for increases in intracranial pressure). [6][7][8][13][15][18] The fact that only 50 % of the patients with alcohol abuse reported a history of headache may be attributable to the presence of cerebral atrophy despite the patients’ younger age or to a certain degree of habituation or tolerance to headache. Seizures as a symptom of CSDH were relatively rare in our study (6.7 %). Gelabert-González et al. observed seizures in 21.4 % of the patients under 40 years of age. [7]

Predisposing factors: haematoma characteristics

Cerebrospinal fluid imbalance

Cerebrospinal fluid imbalance was the most common predisposing factor in our analysis, presenting in 36.1 % of cases. Five of 13 patients developed CSDH following a surgical procedure of the spine with dural opening during which they likely experienced (temporary) CSF hypotension. Three patients with hydrocephalus were treated with a shunt that probably drained too much CSF. The additional outflow of CSF during haematoma formation prevented the build-up of intracerebral pressure, which would have inhibited the formation of extracerebral haematoma. Apart from open procedures involving the CSF system, punctures of the CSF space (lumbar punctures or, for example, placement of an epidural catheter [2][22]) can lead to hypotension and the formation of CSDH (n = 5 of 13 patients in our study).

Disorders of haemostasis

Disorders of haemostasis were present in 33.3 % of the patients with predisposing factors. The use of anticoagulant medications was the most common cause in the group of patients younger than 50 years. Baechli et al. reported that anticoagulants were used by 41 % of the patients with CSDH across age groups. [1] In our study, these patients accounted for only 15 % of the total population of patients, who, however, were of younger age. This finding is in line with the results reported by Gelabert-González et al., who observed a similarly low percentage of young patients with CSDH receiving anticoagulation therapy (12.2 %). [7] Only two patients in our study had a congenital coagulation disorder. It was interesting to note that the rate of patients with CSDH who had no memory of a TBI was higher among young patients with impaired haemostasis (60.0 %) than among patients with other predisposing factors (35.5 %). This finding suggests that less severe TBI can cause the formation of CSDH in patients on anticoagulation therapy compared to patients with other predisposing factors.

Anatomical malformations

In our study, 15 % of the patients with predisposing factors (Group A) presented with an anatomical malformation. The presence of a malformation was the only predisposing factor that was detected in patients under 20 years of age. Intracranial arachnoid cysts were the most common malformation in Group A (88.9 %). Takizawa et al. investigated a group of patients with CSDH who were aged between 7 and 40 years and found that 47.6 % of these patients had an arachnoid cyst. [20] In our study, this percentage is lower (13.3 % of the total patient population), but the mean age of the patients with an arachnoid cyst and CSDH was 32.62 years in our study and 32 years in the study by Takizawa et al.

Alcohol abuse

A history of alcohol abuse was far less common than the presence of CSF imbalance, disorders of haemostasis, and cerebral or cerebrovascular malformations. Only 10 % of the patients with predisposing factors had a history of alcohol abuse, which was thus the least common predisposing factor in our group of patients. Similar low percentages were reported by Liliang et al. [13]

The role of time

The mean time from the onset of signs and symptoms to the diagnosis of CSDH was 17 days for the total patient population in our study. In the literature, however, shorter intervals (e.g. six days [7]) were reported as well. In our study, the time period from onset of symptoms to diagnosis is longer in the group of patients with predisposing factors (20 days) than in the group of patients without predisposing factors (13 days). The time interval from TBI to treatment was 6.53 weeks in the total patient population. This interval is again shorter in Group B (6 weeks) than in Group A (7 weeks). The difference was not significant but the results show a clear trend suggesting a delay in the identification, diagnosis and treatment of patients with predisposing factors.

The reason for the more rapid response to patients without predisposing factors (Group B) may be that these patients received more intensive observation and follow-up since most of them sustained more severe injuries and a more severe TBI than the other patients. By contrast, our data suggest that awareness of the risk of CSDH formation is lower in the management of young patients without a history of a major TBI. To our knowledge, this hypothesis has not yet been proposed in the literature. However, the number of young intensive-care patients who, in everyday clinical settings, are diagnosed with relatively small CSDHs on standard follow-up CT – and who are then followed up more closely as a result of that diagnosis – is remarkably high. At the same time, there appears to be a general willingness to perform diagnostic imaging in young patients who sustained a severe TBI and complain of posttraumatic headache. At least, this willingness to perform imaging in these patients is considerably greater than in young patients who report chronic headaches but have no known history of TBI. This is confirmed by our data and is consistent with our experience in everyday clinical practice.

Conclusions

Young patients too can develop CSDH. If a CSDH is detected in a young patient, it is absolutely important that this patient be assessed for a possible predisposition to haematoma, especially if there is no known history of severe TBI. Young patients with known predisposing factors for CSDH must undergo thorough diagnostic procedures in the clinical setting even if they sustained only a trivial head injury, e.g. during football heading (the true impact of heading in football is often underestimated), especially if a persistent or newly presenting headache is present. In addition, patients and their families should be informed of the predisposition and its consequences and should be made aware of the increased risk of a delayed CSDH even after a mild head injury.

A predisposition to CSDH formation should also be considered in decisions that are made when the medical fitness of individuals with predisposing factors (chronic CSF hypotension, anticoagulant therapy, cerebral malformations) is assessed. In our opinion, military personnel with a predisposition to CSDH should be excluded from certain military duties that are associated with an increased risk of TBI or head accelerations (e.g. parachuting, flying duties, special forces).

References

1. Baechli H, Nordmann A, Bucher HC, Gratzl O: Demographics and prevalent risk factors of chronic subdural haematoma: results of a large single-center cohort study. Neurosurg Rev 2004; 27(4): 263-266. mehr lesen
2. Beck J, Gralla J, Fung C, Ulrich CT et al.: Spinal cerebrospinal fluid leak as the cause of chronic subdural hematomas in nongeriatric patients. J Neurosurg 2014; 121(6): 1380-1387. mehr lesen
3. Catapano JS, Nguyen CL, Wakim AA, Albuquerque FC, Ducruet AF: Middle Meningeal Artery Embolization for Chronic Subdural Hematoma. Front Neurol 2020; 11: 557233. mehr lesen
4. Drapkin AJ: Chronic subdural hematoma: pathophysiological basis for treatment. Br J Neurosurg 1991; 5(5): 467-473. mehr lesen
5. Feghali J, Yang W, Huang J: Updates in Chronic Subdural Hematoma: Epidemiology, Etiology, Pathogenesis, Treatment, and Outcome. World Neurosurg 2020 Sep; 141: 339-345. mehr lesen
6. Fogelholm R, Heiskanen O, Waltimo O: Chronic subdural hematoma in adults. Influence of patient's age on symptoms, signs, and thickness of hematoma. J Neurosurg 1975; 42(1): 43-46. mehr lesen
7. Gelabert-González M, Iglesias-Pais M, García-Allut A, Martínez-Rumbo R: Chronic subdural haematoma: surgical treatment and outcome in 1000 cases. Clin Neurol Neurosurg 2005; 107(3): 223-229. mehr lesen
8. Iliescu IA, Constantinescu AI: Clinical evolutional aspects of chronic subdural haematomas - literature review. J Med Life 2015; 8 Spec Issue(Spec Issue): 26-33. mehr lesen
9. Khadka NK, Sharma GR, Roka YB, Kumar P, Bista P, Adhikari D, Devkota UP: Single burr hole drainage for chronic subdural haematoma. Nepal Med Coll J 2008; 10(4): 254-247. mehr lesen
10. Kunz U, Mauer U, Waldbaur H, Oldenkott P: Früh- und Spätkomplikationen nach Schädel-Hirn-Trauma. Unfallchirurg 1993; 96(11): 595-603. mehr lesen
11. Kutty RK, Leela SK, Sreemathyamma SB, Sivanandapanicker JL, Asher P, Peethambaran A, Prabhakar RB: The Outcome of Medical Management of Chronic Subdural Hematoma with Tranexamic Acid - A Prospective Observational Study. J Stroke Cerebrovasc Dis 2020; 29(11): 105273. mehr lesen
12. Lee KS: Natural history of chronic subdural haematoma. Brain Inj 2004; 18(4): 351-358. mehr lesen
13. Liliang PC, Tsai YD, Liang CL, Lee TC, Chen HJ: Chronic subdural haematoma in young and extremely aged adults: a comparative study of two age groups. Injury 2002; 33(4): 345-348. mehr lesen
14. Mauer UM, Kunz U. Chronisches subdurales Hämatom bei Patienten unter 35 Jahren. Nervenarzt 2007; 78(2): 177-80 mehr lesen
15. Missori P, Maraglino C, Tarantino R, Salvati M, Calderaro G, Santoro A, Delfini R: Chronic subdural haematomas in patients aged under 50. Clin Neurol Neurosurg 2000; 102(4): 199-202. mehr lesen
16. Ohara K, Seki Y, Maeda T, Aiba T: [Primary intracranial hypotension associated with chronic subdural hematoma--report of 2 cases]. No Shinkei Geka 1984; 12(10): 1203-1208. mehr lesen
17. Sambasivan M: An overview of chronic subdural hematoma: experience with 2300 cases. Surg Neurol 1997; 47(5): 418-422. mehr lesen
18. Schebesch KM, Woertgen C, Rothoerl RD, Ullrich OW, Brawanski AT: Cognitive decline as an important sign for an operable cause of dementia: chronic subdural haematoma. Zentralbl Neurochir 2008; 69(2): 61-64. mehr lesen
19. Soyka M: Prevalence of alcohol-induced psychotic disorders. Eur Arch Psychiatry Clin Neurosci 2008; 258(5): 317-318. mehr lesen
20. Takizawa K, Sorimachi T, Honda Y et al.: Chronic Subdural Hematomas Associated with Arachnoid Cysts: Significance in Young Patients with Chronic Subdural Hematomas. Neurol Med Chir (Tokyo) 2015; 55(9):727-734. mehr lesen
21. Tseng JH, Tseng MY, Liu AJ, Lin WH, Hu HY, Hsiao SH: Risk factors for chronic subdural hematoma after a minor head injury in the elderly: a population-based study. Biomed Res Int 2014; 2014: 218646. mehr lesen
22. Vos PE, de Boer WA, Wurzer JA, van Gijn J: Subdural hematoma after lumbar puncture: two case reports and review of the literature. Clin Neurol Neurosurg 1991; 93(2): 127-132. mehr lesen
23. Wan KR, Qiu L, Saffari SE, Khong WXL, Ong JCL, See AA, Ng WH, King NKK: An open label randomized trial to assess the efficacy of tranexamic acid in reducing post-operative recurrence of chronic subdural haemorrhage. J Clin Neurosci 2020; 82(Pt A): 147-154. mehr lesen
24. White M, Mathieson CS, Campbell E, Lindsay KW, Murray L: Treatment of chronic subdural haematomas - a retrospective comparison of minicraniectomy versus burrhole drainage. Br J Neurosurg 2010; 24(3): 257-260. mehr lesen
25. Yang W, Huang J: Chronic Subdural Hematoma: Epidemiology and Natural History. Neurosurg Clin N Am 2017; 28(2): 205-210. mehr lesen
26. Zuckerman SL, Prather CT, Yengo-Kahn AM, Solomon GS, Sills AK, Bonfield CM: Sport-related structural brain injury associated with arachnoid cysts: a systematic review and quantitative analysis. Neurosurg Focus 2016; 40(4): E9. mehr lesen

Manuscript data (article was submitted in German)

Submitted: 30 December 2021

Accepted after revision: 10 April 2022

Citation

Schulz C, Walther C, Hackenbroch C, Mauer UM, Mathieu R: Impact of factors predisposing young patients to the development of intracranial chronic subdural haematoma. WMM 2022; 66(6–7): e5.

DOI: https://doi.org/10.48701/opus4–65

For the Authors

Commander (Navy MC) Assistant Professor Dr. Chris Schulz

Bundeswehr Hospital, Ulm

Department of Neurosurgery

Oberer Eselsberg 40, D-89081 Ulm, Germany

E-Mail: chrisschulz@bundeswehr.org