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Home , Cerebral contusion, Epidural hematoma

대한응급의학회지 제 28 권 제 3 호 � 증례� Volume 28, Number 3, June, 2017

Neurology Lethal Outcome due to Misdiagnosis between Acute and Epidural Expansion after : A Case Report

Jung-Ho Yun, M.D.

Department of Neurological Surgery, University of Dankook College of Medicine, Dankook University Hospital, Cheonan, Korea

Large amount of usually requires surgical intervention. When the amount of epidural hematoma is increasing gradually, causing neurological symptoms, an early emergent surgery may be the only way to prevent lethal outcome. Among many factors associated with the prognosis, age, amount of hematoma, patient's consciousness at the time of admission, and other accompanying injuries are known to be important factors. However, in some cases, symp- toms may be exacerbated due to causes other than the increase in epidural hematoma, such as cerebral infarction. In particular, calcification of the internal carotid is known to be an important factor that causes acute cerebral infarc- tion before and after surgery. Correct identification is important for appropriate treatment between cerebral infarction and cerebral hemorrhage. Herein, we present a case that followed lethal outcome due to misdiagnosis between epidural hematoma expansion and acute cerebral infarction caused by dissection or calcification of the internal carotid artery after blunt trauma. To the best of our knowledge, there have been any reports regarding simultaneous occurrence of acute cerebral infarction and acute epidural hematoma on the same side following blunt trauma.

Key Words: Cranial epidural hematoma, Cerebral infarction, Carotid Artery, Internal, Vascular calcification

acute cerebral infarction5). To our knowledge, there have Introduction been no reports regarding simultaneous occurrence of acute cerebral infarction and acute EDH at the same side Epidural (EDH) are pathologies in which following blunt trauma. the early diagnosis and treatment are important. Additionally, EDH is a variable trauma entity that con- sist of fracture, , subdural Case Report hematoma simultaneously required immediate surgical or medical treatment. The decision to operate is based 56-year-old man who was presented with drowsy men- primarily on the patient’s Glasgow Scale (GCS) tality due to falling down from 5 meters while working score, pupillary abnormalities, and computed tomogra- on the ladder was transferred from another hospital with- phy (CT) parameters, especially clot thickness, in two hours after the accident. The initial vital sign was hematoma volume, , and the status of the within normal range at the time of admission, and there basal cisterns1). Several cases have reported on cases of were no external wounds except swellings of scalp and acute cerebral infarction following the surgery of trau- neck. The patient’s consciousness was alert with normal matic hemorrhage2-4). Also, there were cases of epidural pupil size and light reflex. Also, motor and sensory hemorrhage or subdural hemorrhage in a patient with response was normal by first neurological examination

책임저자: 윤 정 호 충청남도 천안시 동남구 망향로 201 단국대학교병원 신경외과 Tel: 041-550-3921, Fax: 041-550-6369, E-mail: [email protected] 접수일: 2017년 3월 15일, 1차 교정일: 2017년 3월 22일, 게재승인일: 2017년 5월 8일

275 276 / Jung-Ho Yun in emergency room. Prior CT scan showed a small revealed multiple fractures of cervical spine without amount of an EDH at the temporal area with a fracture of abnormal alignment (Fig. 1D and 1E). Two hours after the temporal skull bone (Fig. 1). Cervical spine CT scan injury, we rechecked a brain CT scan with suspicion of

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C D

E Fig. 1. Initial brain computed tomography (CT) scan showed small amount epidural hematoma with in right fronto-temporal area. Cervical CT scan revealed multiple cervical fractures including lamina, spinous process and lat- eral mass fracture. Posttraumatic Cerebral Infarction / 277 increasing hematoma, which revealed a moderate Therefore, we opened dura matter and examined subdur- increasing of the EDH, but not necessary for surgical al space and brain parenchyma, but could not achieve intervention (Fig. 2). However, soon after the follow up or subcortical injury. After the oper- CT scan, the patient’s mental status changed from alert ation, we confirmed the absence of remnant EDH and to stupor showing slow response to verbal and motor other site’s hemorrhage through brain-CT scan (Fig. 3). stimuli and patient’s left side motor was decreased. The patient’s motor and consciousness were gradually However, pupil reflex to light stimulus and vital sign recovered but there were not fully recovery in left side were within normal range. Unfortunately, due to the motor. Six hours after the operation, repeated brain-CT emergent situation eyeball deviation or neglect or aprax- scan revealed low density at left anterior cerebral artery, ia was not documented. We concluded that the patient’s middle cerebral artery territory and midline shifting that neurologic deterioration was acutely induced by the were suggestive of acute cerebral infarction (Fig. 4). We expansion of hematoma which could be conjectured decided on an emergency decompressive craniectomy from the swirl sign in B-CT scan (Fig. 2C) that could not but guardians refused additional operation, so then the be observed in the first CT scan (Fig. 1C). An immediate patients expired 5 days after the first operation due to surgical intervention was decided. In operative finding, severe brain and . we found a moderate EDH with a linear skull fracture but not enough to cause neurological deterioration.

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C Fig. 2. Repeated computed tomography (CT) scan revealed a expansion epidural hematomas with swirl sign (circle) in hematoma internal lesion than initial CT scanning. 278 / Jung-Ho Yun

tion in a neurosurgical center1). Surgical timing is strong- Discussion ly recommended that patients with an acute EDH in coma (GCS score <9) with anisocoria undergo surgical Early recognition and diagnosis of EDH is the key to evacuation as soon as possible1). successfully managing this neurosurgical emergency. However, even when the indications for surgery Patients with EDH can ‘talk and die’ due to rapid expan- described above are not present, an emergency surgery sion of the hematoma6). In surgically treated patients, a may be performed only by neurological deterioration. hematoma volume greater than 50 cm3 is significantly Neurological deterioration are usually caused by a sud- related to higher mortality and unfavorable functional den increase in , which is confirmed with a swirl outcome7). Generally, indications of surgery in traumatic sign radiologically. The swirl sign has been described in EDH are the followings: 1) An EDH greater than 30 cm3 patients with head trauma who have a large extra-axial should be surgically evacuated regardless of the patient’s heterogeneous fluid collection containing both a hyper- GCS score, 2) An EDH less than 30 cm3 and with less attenuating clot and smaller hypo-attenuating region in a than a 15-mm thickness and with less than a 5-mm mid- swirled configuration, which represents active bleeding8). line shift in patients with a GCS score greater than 8 In addition, neurological deterioration could be caused without focal deficit can be managed non-operatively by sudden cerebral infarction, which is well known that with serial CT scanning and close neurological observa- the space-occupying EDH is an important factor in post-

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C Fig. 3. Postoperative computed tomography scan revealed total removal of epidural hematomas without brain compression and no evidence of new hematoma in another lesions. Posttraumatic Cerebral Infarction / 279 traumatic cerebral infarction (PTCI) by Wang et al2). In post-traumatic infarction and the anatomical lesion such this paper, we found that the duration of preoperative as temporo-parietal or temporo-occipital location, vol- brain herniation is the most prominent contributor to ume of EDH and GCS score were the significant risk

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C D Fig. 4. Postoperative computed tomography (CT) scan demonstrated low density with midline shiting at right fronto-temporo parietal lesion which indicated as cerebral infarction. Bone density CT scan confirmed the calcification of internal carotid artery (circle).

Table 1. Literature review of PTCI with moderate or severe TBI Case no. Developing time No Literatures/year Severity Risk factors associated with PTCI (incidence) (median) 1 Wang et al.2)/2014 32 (18%) - Severe Anatomical location, volume, preop shock, duration of preop brain herniation, low GCS 2 Liu et al.3)/2015 18 (26%) 1 day Severe Hyperthermia, tSAH, thrombocytopenia, hemocoagulative disturbance 3 Tian et al.4)/2008 42 (12%) 8.7 days Moderate & severe Low GCS, , brain herniation, decompressive craniectomy 4 Chen et al.9)/2013 28 (10%) <12 hours Moderate & severe Low GCS, thrombocytopenia, abnormal PT, elevated D-dimer, DIC PTCI: posttraumatic cerebral infarction, TBI: , GCS: , tSAH: traumatic subarach- noid hemorrhage, PT: prothrombin time, DIC: disseminated intravascular coagulation 280 / Jung-Ho Yun factors for PTCI. of PTCI require a high degree of clinical suspicion. There are several studies about PTCI following a blunt Symptoms such as neglect, eyeball deviation and (Table 1). In our case, we determined that it apraxia are generally more prominent than symptoms by was exacerbated by EDH expansion rapidly before the brain compression such as motor deficit, pupil abnormal- operation. However, we thought that it might not be after ity and when symptoms are aggravated confirming that there is no brain compression in opera- by cerebral infarction. However, it is not easy to distin- tive finding. The reasons we think that this patient is dif- guish between patients with head trauma only by neuro- ferent from the case of cerebral infarction due to direct logical examination whether the symptoms are exacer- compression by EDH or posttraumatic vasospasm are as bated by cerebral hemorrhage or if the symptoms are followings. First, there were not severe brain compres- exacerbated by cerebral infarction. In particular, it is not sion by EDH in operative finding and we performed easy to diagnose acute cerebral infarction without clini- early operation before brain herniation. Therefore, we cal suspicion because it is difficult to detect abnormali- believe that our case do not include direct compression ties in the CT scan and the delay in presentation of caused by postoperative cerebral infarction which is sig- symptoms at the initial stage of acute cerebral infarction. nificant associated with direct pressure effect by EDH Therefore, if a patient with a blunt trauma to the neck as itself or the long duration of brain herniation2,10). Second, in our case has a calcification of the internal carotid postoperative CT scan revealed low density at internal artery, it should always be suspicious and aware that carotid artery (ICA) (including anterior cerebral artery, symptoms may be exacerbated by acute cerebral infarc- middle cerebral artery) territory, not posterior cerebral tion. After operation, it is necessary to match between artery or middle cerebral artery territory that generally operative finding and radiologic finding and symptom developed in PTCI2). Also, the CT scan showed bilateral deterioration. In an era where radiologic examinations carotid calcification and the patient had an external can be carried out swiftly without much time delay, we wound by blunt trauma on the patient’s neck. Our other believe that exact physical examination should be the report presented a case that diagnosed acute cerebral first priority at the emergency room and radiological infarction after complete occlusion of ICA due to blunt examinations should act as supportive measures to con- head trauma11). In this report, we suggested that patient firm the physical examination. with ICA calcification might tend to be developed to acute cerebral infarction after head and neck blunt trau- ma. Also, several cases with similar mechanism as this Conclusion report have been shown regarding acute cerebral infarc- tion followed by traumatic ICA dissection12). Third, there The deterioration of neurological symptoms due to was no decrease in blood pressure before or after the sudden increasing of EDH are an important indication of operation and there were not present trauma induced the surgical treatments. However, as in the case , which it is generally followed by posttrau- described above, it is necessary to distinguish symptom matic vasospasm developed approximately 8 days after aggravation due to acute cerebral infarction in patients trauma3,13). with calcification in ipsilateral ICA after blunt trauma One important aspect we can learn from this case is and symptom aggravation due to sudden increasing of that we need to diagnose and judge more precisely for EDH as like swirling sign in brain CT scan. Recently, causes of neurological deterioration. To do this, it is nec- there is a very desirable phenomenon to perform imme- essary to check the amount of bleeding through repeti- diate surgical treatment as soon as possible for patients tive CT scan when symptoms change, or try to find out with traumatic hemorrhage requiring the operation after the other causes. Tian et al4) reported that initial recogni- the introduction of trauma centers in several hospitals. tion by physicians is often difficult because of the However, it should be noted that when treating patients diverse clinical manifestations, the delay in presentation with risk factors for cerebral vessel disease such as dia- of symptoms, and other associated brain injuries. betes, , hyperlipidemia and calcified or ath- Therefore, early diagnosis and successful management erosclerotic ICA, a high degree of clinical suspicion is Posttraumatic Cerebral Infarction / 281 first step to examine neurologic change exactly in emer- patients with moderate or severe head trauma. Neurosurg gency room for excluding cerebral infarction. Rev. 2008;31:431-7. 05. Borger V, Schuss P, Kinfe TM, Vatter H, G?resir E. Decompressive craniectomy for : early cranioplasty is a predictor for postoperative complications. World Conflict of Interest Neurosurg. 2016;92:83-8. 06. Zakaria Z, Kaliaperumal C, Kaar G, O’Sullivan M, Marks The author reports no conflict of interest concerning C. Extradural haematoma to evacuate or not? Revisiting materials used in this study or the findings specified in treatment guidelines. Clin Neurol Neurosurg. 2013;115: this paper. 1201-5. 07. Lee EJ, Hung YC, Wang LC, Chung KC, Chen HH. Factors influencing the functional outcome of patients Acknowledgments with acute epidural hematomas: analysis of 200 patients undergoing surgery. J Trauma. 1998;45:946-52. The present research was conducted under a research 08. Zimmerman RA, Bilaniuk LT. Computed tomographic staging of traumatic epidural bleeding. 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