In order to elucidate the sequential changes of severe injury / severe head injury in Sendai City and Miyagi Prefecture, the ambulance transportation data of Sendai City Fire Bureau (SCFB) and Miyagi Neurotrauma Data Bank (Miyagi) were retrospectively analyzed during 1992 – 2008 and 1995 – 2006 respectively. The results showed 1) the number of injured patients transported by ambulance of SCFB showed its peak in 2004, then it has been decreasing. Among them, the number of severely injured patients begun to decrease since 1999. 2) The number of severely injured patients due to motor vehicle accidents has sharply decreased; about 1/3 in the past 17 years. 3) The number of ambulance transportation due to motor vehicle accidents has decreased in the age of 20 – 39. 4) The number of ambulance transportation of severely injured patients caused by general injury was stable in the past 10 years, but those by self-injury increased sharply until 2000 and have not been decreased since then. 5) Miyagi showed the number of hospital admission of head injured patients due to motor vehicle accidents has decreased since 2002, and this decrease was evident in the age of 10 – 29. Among them, the number of severe head injury with GCS < 9 has decreased since 2003, whereas the number of hospital admission of head trauma patients due to fall or fall from the height has decreased only slightly. In conclusion, severe head injury has been decreasing in Sendai City / Miyagi Prefecture, and its main cause is decrease in motor vehicle accidents in the younger generation especially.
In spite of expectation that brain hypothermia (HYPO) will have a protective effect on the traumatic brain injury (TBI) in children, recent Phase III study has concluded no benefit in HYPO for pediatric TBI. This study prompted us to review our pediatric TBI patients treated with HYPO to determine its feasibility, safety, and efficacy. All patients were monitored in the intensive care unit for complications and assessed by Glasgow Outcome Scale at 3 months. Since 1995, 24 children (range, 1 to 17; mean, 10.1 years old) with severe TBI (Glasgow Coma Scale [GCS] score ≤ 8; mean, 5.6) were cooled to 34˚C and maintained at least 48 hours, thereafter rewarmed 1˚C/day. The median time from injury to initiate cooling was 107.5 minutes (range, 54 to 2980 minutes) and to reach 34˚C was 218.5 minutes (range, 72 to 3310 minuets). Overall, 58% of the patients had an unfavorable outcome (defined as severe disability [SD], vegetative state [VS], or death [D]) and mortality rate was 25%. Concerning 12 patients in the later study period, an unfavorable outcome was 33% and no mortality was recorded. There were 3 Ds and 1 VS. Two Ds in infant were due to refractory increase of intracranial pressure during hypothermia, whereas delayed brain swelling after rewarming caused 1 D and 1 VS in older children. There were no serious complications to discontinue hypothermia treatment or to be related to poor outcome. Child brain is vulnerable to insult. Prolonged hypothermia may be necessary to regulate intracranial pressure. Advancement of systemic management and neuromonitoring together with accumulated knowledge and technical innovation in hypothermia treatment enable us safer and more effective achievement of brain hypothermia treatment.
Growing skull fracture (GSF) is well known but rare complication that can occur in infants and young children. The principle concept of treatment for GSF was simple, but detailed methodology for surgery is still controversial especially in infantile cases. GSF can be a challenging surgical problem facing the pediatric neurosurgeon.
We presented an 8-month-girl exhibited her left parietal bulging after head injury four months later. CT and MRI findings demonstrated typical widened fracture (20 mm ¥ 65 mm) and leptomeningeal cyst. We repaired dural defect with autologous periostium and cranial defect with vascularised bone flap. It was very useful to use absorbable plate and screw system for rigid cranial fixation. Our surgical concept for GFS in younger children is not to use foreign materials and make sure cranial fixation as soon as possible.
We report infantile subdural hematoma caused by abuse. Between January 2006 and December 2009, 10 cases of definite and highly suspicious abusive subdural hematoma in infants were treated at Nara Medical University Hospital. The mean age was 5.4 months. On CT examination, severe cerebral swelling was seen in 8 (80%) and wide spreading cerebral ischemia and atrophy in 9 (90%). Retinal hemorrhage was commonly seen in this series (90%). Subdural drainage and/or subdural-peritoneal shunt surgeries were performed in 6 cases, and intensive combined therapy of mild hypothermia and barbiturate was adapted in 7 cases. Favorable outcome was achieved in only 3 cases. In spite of aggressive treatment, clinical outcome are still bad. In our series, assailants were predominantly not father but mother. There were various and complex factors for child abuse. Cautious insight and suspicion are necessary to detect abusive injuries in infants. It is very important to endeavor to prevent recurrences of abusive injuries.
Objective: To assess the impact of presenting tachycardia on emergency department (ED) arrival for multiple trauma patients with severe traumatic brain injury (TBI).
Materials and Methods: Using retrospective analysis at our Level I trauma center between 2007 and 2009, we identified blunt multiple trauma patients who had severe TBI, which was defined as an abbreviated injury score (AIS) ≥4. Tachycardia was defined as a heart rate (HR) of ≥100 bpm. Patients who were <15 years of age, in cardiac arrest on arrival, those having spinal cord injury, uncontrolled arterial fibrillation, chronic heart failure or hemorrhagic shock were excluded. Outcome was investigated using the Glasgow Outcome Scale at hospital discharge. Two study groups, “good outcome” (GO; good recovery or moderate disability) and “worse outcome” (WO; severe disability, considerable vegetative state, or death) group were compared.
Results: 643 patients had head injury and 34 patients had severe TBI with multiple injuries. Mean injury severity score (ISS), shock index, and revised trauma score (RTS) were 31 ± 8, 0.59 ± 0.2, and 6.44 ± 1.3, respectively. Median Acute Physiology and Chronic Health Evaluation (APACHE) II score was 22. Ten of 34 patients were tachycardiac on ED arrival. In the WO group, the number of patients with tachycardia, Glasgow Coma Scale <9 patients, mean RTS, and APACHE II scores were higher than those in the GO group. Multivariate logistic regression analysis showed that presenting tachycardia and an APACHE II score of >22 were independent predictors of worse outcome (odds ratio, 17.6 and 27.7, respectively).
Conclusion: Presenting tachycardia on ED presentation is a crucial parameter for worse outcomes in trauma patients, who will develop worse outcome, with severe TBI suffering form non-hemorrhagic shock. Further studies of pharmacological stabilization using b-blockers during primary resuscitation and their effect on cerebral metabolism are warranted.
Objectives: This study investigated the effect of preexisting antithrombotic therapy on the rate of hematoma enlargement or thromboembolic event and outcome in patients with traumatic intracranial hemorrhage (TICH).
Method: A retrospective review of 152 patients with TICH age 60 years and older was performed. Thirty-nine patients with TICH receiving antithrombotic therapy (ATT group) were compared with a control group of 113 patients with TICH but not taking any antithrombotic agent. ATT group consisted of anticoagulation therapy group (n=13) and antiplatelet therapy group (n=26). Age, gender, Glasgow coma scale (GCS) on admission, type of intracranial hemorrhage, symptomatic hematoma enlargement, thromboembolic event and Glasgow outcome scale (GOS) at discharge were investigated.
Results: No statistically significant differences were found between the two groups in terms of age, gender, GCS and type of intracranial hemorrhage. Incidence of symptomatic intracranial hematoma enlargement was significantly higher in patients receiving antithrombotic therapy compared with patients without antithrombotic therapy (30.8% vs. 6.2%; p<0.01). In the antithrombotic therapy group, the anticoagulation therapy group and the antiplatelet therapy group had a significantly high incidence of hematoma enlargement at 38.5% and 26.9% respectively. Rate of the in-hospital thromboembolic event was significantly higher in patients taking antithrombotic agent than in those not taking antithrombotic agents (17.9% vs. 0.9%; p<0.05). In the anticoagulation therapy group, 5 of 13 patients (38.5%) developed thromboembolic complications, whereas 2 of 26 patients (7.7%) taking antiplatelet developed. Hospital mortality in TICH patients receiving antithrombotic therapy was significantly higher than in the control group (30.8% vs. 11.5%; p<0.05).
Conclusion: Preinjury antithrombotic therapy appears to be associated with a risk of thromboembolization and high mortality after traumatic brain injury. The anticoagulation therapy group is more likely to develop thromboembolic complications than the antiplatelet therapy group.
Minor head and cervical injury have been reported to precipitate thoracic outlet syndrome (TOS). We have performed surgery for forty-nine patients with TOS. The surgical methods consisted of a transaxillary approach for the first rib resection (FR), an anterior approach for scalenectomy (AAS), and a lateral approach for scalenectomy (LAS).
We evaluated the effect of minor head and cervical injury on TOS. An obvious history of minor head and cervical injury preceding TOS was noted in five of forty-nine patients. We present surgical findings in three of five traumatic cases. All cases underwent LAS. Preoperative symptoms disappeared or improved immediately.
In a previous report of surgical findings in traumatic brachial plexus injury, hematoma and scar formation were observed in around the brachial plexus. In our series, however, neither hematoma nor scar formation was found in the surgical field. In one case, there was a variation of the middle scalene muscle, while in another case, a variation of the superficial muscle tendon was observed.
TOS manifests various symptoms such as pain, paresthesia, weakness, swelling, coldness and pallor. These symptoms were confused in patients with minor head and cervical injury. In diagnosing TOS following trauma, we think that differentiation from minor head and cervical injury is important.
We have performed burr hole surgery in the emergency room for severe acute subdural hematoma from April 2007 in twenty five patients. All patients were deep comatose and showed cerebral herniation sign with bilateral pupillary abnormalities. Burr hole surgeries were performed as soon as possible after CT evaluation. Continually decomporresive craiectomies were followed if clinical improvements were achieved and mild baribiturate-moderate hypothermia combined (MB-MH) therapy was induced postoperatively in some cases. The mean average was 65.6 years (range 16 – 93). The causes of head injuries were traffic accident in 9, fall down in 13 and unknown in 3. The mean GCS on admission was 4.4 (range 3 – 9). The mean time interval from arrival to burr hole surgery was 33.5 minutes (range 21 – 50 minutes). Decompressive craniectomy was indicated in 14 cases and MB-MH therapy was induced in 13 cases. The overall clinical outcome consisted of good recovery in 3, moderate disability in 2, severe disability in 3, persistent vegetative state in 3 and death in 14. Favorable results can be expected even in patients with serious acute subdural hematoma. Emergent burr hole surgery was effective to decrease intracranial pressure rapidly and to save time. So active burr hole surgery in the emergency room is strongly recommended to all cases of severe acute subdural hematoma.
Golf is a popular sports activity which people of all ages can enjoy. Use of Golf cart for moving around golf course is commonly. However power of golf cart is stronger than most people think, its driving is at potential risk. Injury accident due to its driving error occurs in Japanese men's golf tour is still fresh in our mind. Recently we experienced two cases having golf cart related head injury.
Case 1 was thrown out of passenger seat of golf cart and was hit hard on head and face in foreign golf course. She was transferred to our hospital to receive medical treatment and was diagnosed as cerebral contusion on bilatelal frontal lobe.
Case 2 was also thrown out of passenger seat of golf cart and was hit hard on occipital and temporal. Because of progressing consciousness disturbance, He was transported to our hospital by ambulance helicopter. His conscious level score was III-200 using Japan coma scale, 6 using Glasgow coma scale. His CT scan presented severe bilateral frontal contusion and left acute subdural hematoma. In spite of emergency operation, he became persistent vesitative state unfortunately.
The number of golf cart related head injury is little, but it caused severe head injury required neurosurgical management in some cases. At this point safety standards for golf cart in our country is not established. Preventing miserable accident, it is necessary to establish safety system including equipment of seatbelt and widespread of high-security golf cart.
Recently we treated an unusual case of acute subdural hematoma (ASDH) caused by ruptured dural arteriovenous fistula (dural AVF) immediately following traumatic head injury. A 21-year-old male presented headache and tinnitus after bumping into another player in a basketball game, and falling to the floor. Upon admission his consciousness was alert and no neurological deficit was apparent. CT scan revealed ASDH in the left convexity without any parenchymal lesion. Since the circumstances of the incident of head trauma seemed too minor to cause ASDH, digital subtraction angiography (DSA) was subsequently performed. DSA revealed a small aneurismal sac in the left convexity. The sac was fed by the left middle meningeal artery and the right occipital artery suggested dural AVF. Subsequently craniotomy was performed to extirpate the vascular anomaly to prevent recurrent hemorrhage. During the operation a small vascular assembly on the inner surface of the convexity dura matter was discovered. This lesion was adhering tightly to the thickened arachnoid, and was totally resected with surrounding normal dura mater. Pathological examination revealed broken internal elastic lamina, groups of abnormal vessels, and older hemorrhagic scar tissue. All of these are compatible findings to dural AVF and its rupture. Post-operative angiography confirmed complete absence of dural AVF.
Although some vascular anomalies such as cerebral aneurysm, middle meningeal artery aneurysm, or cerebral AVM are known to lead to ASDH, dural AVF as a cause of ASDH is extremely rare, with only a few reported cases.
It is not clear why the dural AVF ruptured after minor traumatic head injury, but it is suggested that shearing strain may damage the adhesion between the dural AVF and arachnoid, or that increase of venous pressure at the instance of traumatic incident may result in rupture of the dural AVF. Cerebral angiography is mandatory in the patient presenting unexplained ASDH.
A 2-month-old boy presented with infected subdural hemorrhage manifesting as sustained fever and seizures. The boy had been well without contributory medical history. Physical examination found no neurological impairment with intact superficial appearance. The parents reported no recent trauma or shaking injury. Blood examination was normal except for white blood cell count of 19200/µl and C-reactive protein level of 6.7 mg/dl. Bacterial culture of nasal swab, urine, stool, and venous blood samples was negative. Cerebrospinal fluid examination showed normal findings. Cranial computed tomography revealed an expansive subdural fluid collection in the right frontotemporal region. Magnetic resonance imaging showed the lesion as heterogenous intensity on T1- and hyperintensity on T2-weighted images with intense enhancement of the outer membrane. The patient underwent burr-hole drainage, which identified an encapsulated subdural hematoma, intermingled with pus material. Culture of the pus identified Escherichia coli (E. coli). The patient received antibiotic therapy for 8 weeks that resulted in complete resolution of the infection. We assumed that preexisting subdural hematoma arising after unrecognized minor head trauma was hematogenously infected by E. coli. Infected subdural hematoma should be assumed as differential diagnosis in infants presenting with subdural hemorrhage and bacteremia.
A 6-year-old boy after a fall of 3 m was brought to our hospital. Computed tomography (CT) scan detected right temporal subdural hematoma and temporal bone linear fracture. The depth of hematoma was 5 mm. He experienced vomiting and transient amnesia. One day after head injury, the subdural hematoma had not changed, but a high density area appeared in the transit portion from right transverse sinus to right sigmoid sinus, and thereafter both size and density of the area increased. Three days after the head injury, enhanced CT showed the empty delta sign, but he was free of symptoms such as nausea, headache and transient amnesia. Therefore, we diagnosed this patient as having asymptomatic cerebral venous sinus thrombosis associated with head injury. Magnetic resonance imaging (MRI) showed contusion in the right temporal lobe, but there was no edematous lesion around the cerebral venous sinus thrombosis. We treated him conservatively. Eleven days after the head injury, the thrombosis was diminished on MRV. Fifteen days after the head injury, enhanced CT showed disappearance of the thrombosis. Eighteen days after the head injury, he was discharged without any neurologic deficits.
Chronic subdural hematoma (CSDH) can usually be treated by burr-hole craniostomy with closed-system drainage. In some cases repeated craniostomies are needed for persistent recurrences, and wide membranectomy via craniotomy will be additionally needed in some selected cases. In this report, we present a case of organized chronic subdural hematoma with extensive intra-membranous hemorrhage, which occurred 1 year after the initial burr-hole craniostomy. A seventy-six year-old man was referred to our hospital with mild dysarthria and left hemiparesis on November 2, 2008. After the initial burr-hole craniostomy on November 5, 2008, craniostomies were repeated four times until his fifth admission on October 9, 2009. Only 2 weeks after the fifth burr-hole craniostomy, the hematoma had expanded to the initial pre-operative size, and membranectomy under extensive craniotomy was performed under general anesthesia. A thickened outer membrane with several hemorrhagic foci was extensively resected. Histologically, the membrane appeared similar to the usual membrane encountered in CSDH with extensive infiltration of inflammatory cells and several hemorrhagic foci. Membranectomy with extensive craniotomy has been reported to be beneficial for organized CSDH; however, peri-operative complications must be considered with elderly patients. The existence of multiple trabeculae under endoscopy, and enhancing extensive membranes seen on MRI, should be the trigger to consider early membranectomy to avoid further recurrences of CSDH.
We report a 59-year-old man who got blunt injury of head and face by 200 kg container. His Japan Coma Scale score on admission was one and Glasgow Coma Scale score was 14. He had paresis of bilateral oculomotor nerves and left abducens nerve, and facial numbness of the left V1–3 territories. CT scan showed traumatic subarachnoid hemorrhage, cerebral contusion and pneumocephalus. Fracture of bilateral temporal bone, left petrous bone and the mandible was observed. Angiography showed bilateral dissection of the petrous portion of the internal carotid artery and left carotid-cavernous fistula. Follow-up angiography and MRA showed disappearance of the arterial dissection and carotid-cavernous fistula. He was treated conservatively and discharged with left facial numbness and left abducens palsy.