Diffuse axonal injury produces an early and sustained deterioration of the level of consciousness (as mentioned in the case statement) without a lesion on CT scan to justify the picture. Sometimes, punctate hemorrhages at the level of the corpus callosum, corticosubcortical junction and dorsolateral portion of the brainstem are evidenced in this imaging test.

After a traffic accident a 38-year-old patient is admitted to the ICU in coma. After several days the patient does not improve neurologically and a CT scan shows hemorrhagic punctate lesions in the corpus callosum and cortico-subcortical junction. What is the diagnosis?

[Clinicopathological studies of diffuse axonal injury--five autopsy cases].

In severe head injuries, delayed intracerebral hematoma appearing lately is noted due to the spread use of serial CT scan. The authors experienced the autopsy of 5 cases who presented diffuse axonal injury (DAI) among these new lesions in repeated CT scan findings and report the pathohistological findings. Subjects were as follows: The age range of the patients was 15 to 25 years. The consciousness levels of the 5 cases on admission were 6 or less by the Glasgow coma scale. CT findings of DAI were revealed hemorrhage of the corpus callosum, basal ganglia, tegmentum of pons, intraventricular, and acute brain swelling. Total clinical courses were 2 to 29 days, but most of them were 9 or less days. In the macroscopic findings, marked congestion and edema revealed mainly in deep part of the white matter of the frontal lobe in all 5 cases. Callosal disruption and hematoma adjacent the corpus callosum revealed in 4 out of 5 cases. Cerebral contusion with hemorrhage revealed in 3 out of 5 cases. Intraventricular hemorrhage and traumatic subarachnoid hemorrhage revealed in 2 out of 5 cases. Hemorrhage of basal ganglia and base of pons revealed in 2 cases. Microscopic examination of all 5 cases revealed pallor of myelin in the corpus callosum and white matter surrounding hemorrhagic lesion, and abnormal tortuous, swelling and fragmentation of axons in stained preparation. Axonal retraction ball was recognized in 3 out of 5 cases. In conclusion, five autopsied cases who presented acute brain swelling and hemorrhage of corpus callosum and tegmentum of pons in serial CT scan were examined.(ABSTRACT TRUNCATED AT 250 WORDS)

[Clinical features and CT diagnostic criteria for diffuse axonal brain injury].

The clinical and computed tomographic features of 117 patients with severe closed head injury were analysed. We put forward the CT diagnostic criteria of diffuse axonal injury (DAD)i.e. (1) single or multiple small intraparenchymal hemorrhages in the cerebral hemispheres (< 2 cm in diameter); (2) intraventricular hemorrhage; (3) hemorrhage in the corpus callosum; (4) small focal areas of hemorrhage adjacent to the third ventricle (< 2 cm in diameter); (5) brain stem hemorrhage. Our patients were divided into DAI group and non-DAI group according to the set of criteria. Traffic accidents were the main injury cause in patients with DAI. GCS on admission in patients with DAI were significantly lower than those in patients without DAI. The incidence of diffuse brain swelling in patients with DAI significantly higher than that in non-DAI patients, whereas the incidences of skull fracture and epidual hematoma were respectively significantly lower than those in non-DAI patients. There was no significant difference between the incidences of subarachnoid hemorrhage and subdual hematoma in the two groups. The incidence of poor outcome in DAI group was significantly higher than that in non-DAI group, although there was no significant difference between the mortalities in the two groups. Because DAI is a very important factor worsening the outcome of head-injured patient, it is very important to make a diagnosis as soon as we can. However, the clinical manifestations of DAI are not specific and DAI does not show directly on CT, so it is difficult to make a diagnosis. The CT diagnostic criteria of DAI we put forward now are practicable, though they are not perfect.

[An autopsy case of traumatic subdural hematoma from arterio-venous malformation with diffuse axonal injury].

Diffuse axonal injury (DAI) is defined as widespread damage to axons in the white matter of the brain without focal injury such as contusion and acute subdural hematoma. A case of traumatic subdural hematoma from arterio-venous malformation accompanied by DAI is reported. A 58-year-old man was assaulted, and immediately lost consciousness, and remained unconscious during about 44 hours until his death. The autopsy revealed acute subdural hematoma (about 160 g) on left temporal lobe and left cingular, uncal and cerebellar tonsillar herniation, and tear and hemorrhage of the corpus callosum. Under this subdural hematoma, gray-whitish vascular lesion with subarachnoid hemorrhage was found. Histologically, this lesion was diagnosed as the arterio-venous malformation. Neuropathological examination of the corpus callosum, dorsolateral part of midbrain and superior cerebellar peduncle revealed DAI findings, such as swelling and ballooning of the myelin fibers, swelling and waving of axons, and retraction balls. Axon degenerations were also observed immunohistochemically by anti-200 kD neurofilament antibody. From the results, his unconsciousness from the moment of impact might be occurred from not only subdural hematoma but also DAI.

[Two cases of delayed posttraumatic vasospasm followed by brain SPECT].

This is a report of two cases of delayed posttraumatic vasospasm. In case 1, a 68-year-old male was injured by falling. He did not show any neurological deficits on admission. CT scan revealed a diffuse subarachnoid hemorrhage (SAH) without brain contusion. Aneurysm was not disclosed by angiography. On the 7th day after admission, he presented disorientation. Reviewed angiography revealed diffuse delayed vasospasm. 123I-IMP brain SPECT showed an extensive low perfusion area in the bilateral parietal portion. In case 2, a 71-year-old female experienced immediate development of a deep comatose state after head injury. CT scan on admission disclosed a massive acute left subdural hematoma and the severe compression of the left cerebral hemisphere by the hematoma. But traumatic SAH was not diffuse and was restricted to the left basal cistern. After emergency operation, her consciousness level improved and the mass effect of the subdural hematoma was diminished. On the 7th day after the operation, her neurological condition worsened. CT scan showed some infarction lesions in the left cerebral hemisphere and mild left cerebral swelling. Angiography on the same day revealed vasospasm in M2-M3 portion of left middle cerebral artery. HM-PAO brain SPECT disclosed low perfusion in the left parietal region, but a state of high perfusion in the other region. In case 1, vasospasm might have been derived from diffuse clots of traumatic SAH caused by the same process as postruptured aneurysmal vasospasm. In case 2, the region of vasospasm was not associated with traumatic SAH. It corresponded to the site of the brain contusion. It was suggested that the cause of vasospasm might have been the direct mechanical injury to the arterial wall and chemical substances deriving from the contused brain tissues. We conclude that SPECT or transcranial Doppler monitoring should be used for the early detection of posttraumatic vasospasm.

[A clinical and pathological study of diffuse axonal injury].

There is increasing evidence from human and experimental studies that the most important factor governing the outcome in head injury is the severity of diffuse axonal injuries. The authors have experienced 18 cases of severe diffuse axonal injury which showed post-traumatic coma for more than 24 hours and CT findings resembling those of shearing injuries of the cerebral white matter such as have been presented by Zimmerman et al. (1978). The consciousness levels on admission were 6 or less on the Glasgow Coma Scale and all cases were shown clinically to have primary brain stem injury. The main type of head trauma resulted from road traffic accidents (83%). Skull fractures were found in only 5 cases (28%). These findings suggested that acceleration/deceleration injury produce in the patients severe diffuse axonal injury. Initial ICP was below 20 mmHg in 11 cases out of 13 (85%). Parenchymal small hemorrhagic lesions of initial CT were basal ganglia (7 cases), corpus callosum (4 cases), pons (4 cases), midbrain (3 cases) and thalamus (2 cases). Extraparenchymal hemorrhagic lesions included intraventricular hemorrhage (6 cases) and subarachnoid hemorrhage (6 cases). Two autopsied cases of severe diffuse axonal injury (acute case and chronic case) showed remarkable congestion and edema in the deep part of the frontal white matter. Microscopic examination revealed marked axonal degeneration including axonal retraction ball in the corpus callosum, in the internal capsule and in the white matter of the brain stem. Glasgow Outcome Scale of the 18 patients at 3 months after the trauma made us concerned that no patients indicated good recovery or even only moderate disability.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical studies on diffuse axonal injury in patients with severe closed head injury.

To discuss the clinical criteria for diagnosing diffuse axonal injury (DAI). Clinical and computed tomographic features of 117 patients with severe closed head injury were analyzed. The authors preliminarily put forward CT diagnostic criteria of DAI, that is, 1) single or multiple small intraparenchymal hemorrhages in the cerebral hemispheres (< 2 cm in diameter); 2) intraventricular hemorrhage; 3) hemorrhage in the corpus callosum; 4) small focal areas of hemorrhage adjacent to the third ventricle (< 2 cm in diameter); and 5) brain stem hemorrhage. All patients were divided into two groups, DAI and non-DAI group, according to the criteria. There were 42 patients in the DAI group and 75 patients in the non-DAI group. The injury causes, Glasgow coma scale (GCS) scores on admission, coexisting injuries and outcomes were compared between the two groups. The relationship between DAI and the outcomes in the patients with severe head injury was analyzed. Traffic accident was the main injury cause in the cases of DAI. GCS scores on admission in patients with DAI were significantly lower than those in patients without DAI. The incidence of diffuse brain swelling (DBS) in the DAI group was significantly higher than that in the non-DAI group, whereas the incidences of both skull fracture and epidural hematoma (EDH) in the DAI group were significantly lower than those in non-DAI group. There was no significant difference between the incidence of subarachnoid hemorrhage (SAH) and subdural hematoma (SDH) in the two groups. The incidence of poor outcome in the DAI group was significantly higher than that in the non-DAI group, although there was no significant difference between the mortalities in the two groups. Because DAI is a very important factor worsening the outcome of patients with head injury, it is essential to make a diagnosis as soon as possible. The clinical manifestations of DAI, however, are not specific and DAI does not show directly on CT scans, so it is difficult to make a definite diagnosis. The CT diagnostic criteria of DAI put forward in this article are practicable, though they are by no means perfect.

[Epidemiology of head traumas. "Barcelona" data base. Objectives, design and analysis of 584 cases].

Descriptive analysis of some features in patients with cranio-encephalic traumatisms (CET) admitted to our hospital and collected in a data base, in order to establish the prognosis of the lesions and apply the most appropriate diagnostic and therapeutic procedures. Since July 1987 to June 1989 we collected data on 584 patients with CET who presented the following selection criteria: consciousness level lower than 13 points in the Glasgow scale and/or pathologic computerized tomography. According to the consciousness level (Glasgow scale) on admission, patients were classified into three groups: slight CET (Glasgow 15-13), moderate CET (Glasgow 12-9), and severe CET (Glasgow < 9). The traumatic mechanisms were divided into 8 categories (occupant, pedestrian, motorbike, aggression, labor, drop, sporting, cyclist). According to the main lesion we considered the following diagnoses: subdural hematoma, epidural hematoma, cerebral contusion (s), diffuse lesion with normal computerized tomography and/or subarachnoid hemorrhage, cerebral congestion, and diffuse axonal lesion. Results were evaluated six months after using the Glasgow scale. The mean age of patients with slight CET was 37.7 +/- 22.1 years, those with moderate CET 31.7 +/- 22.6 years, and those with severe CET 30.8 +/- 21.6 years. Four hundred and forty-two were men (75.6%). The time period between the accident and hospital admission could be determined in 512 cases (87.6%). Severe CET arrived to the hospital (4.8 +/- 7.3 hours) earlier than the other groups (6.6 +/- 11.9 hours in moderate CET and 14.2 +/- 23 hours in slight CET). Most of patients, 488 (83.5%), were referred from another hospital, whereas the remaining cases came directly from the accident place. Traumatic mechanisms according to the previous categories were: occupant 145 (25%), pedestrian 112 (20%), motorbike 104 (18%), cyclist 2 (0.003%), labor 39 (7%), drop 154 (27%), sporting 7 (1%), aggression 10 (2%). Percentage of traffic accident was higher in patients with severe CET (74.6, 64, and 47% in severe moderate, and slight CET, respectively). The main lesions were: acute subdural hematoma, 72 (12.3%); cerebral contusion, 207 (35.4%); epidural hematoma, 88 (15%); normal computerized tomography/subarachnoid hemorrhage, 87 (14.8%); swelling, 17 (2.9%); diffuse axonal injury, 74 (12.6%); and the remaining, 39 (6.6%) had other lesions such as hydrocephalus fracture-sinking, etc. Mortality was 44.2, 12.2, and 3.7% respectively in severe, moderate, and slight CET. Data base may contribute to establish the prognosis of CET and to determine the efficacy of therapeutic procedures as well as that of diagnostic and investigational methods.

[Bilateral traumatic hemorrhage in the basal ganglia: report of two cases].

Hematomas of the basal ganglia in head injury have long been recognized by pathologists with an interest in head injury but their mechanism has not been revealed clearly. We report two cases of bilateral traumatic hemorrhage in the basal ganglia. Case #1, a 17-year-old male was admitted to our hospital immediately after a traffic accident. Neurological examination revealed that the patient was comatose and had right hemiparesis. CT scan showed bilateral hemorrhage of the basal ganglia and subarachnoid hemorrhage in the perimesencephalic cistern. MRI showed high signal intensity areas in the bilateral basal ganglia, perimesencephalic cistern, cerebral white matter and corpus callosum. The patient was diagnosed as having diffuse axonal injury coinciding with bilateral hemorrhage of the basal ganglia. Stereotactic aspiration for the hematoma of the left basal ganglia was carried out. Case #2, a 75-year-old male was admitted immediately after falling from the roof of his house. Neurological examination revealed no neurological deficit except for headache and nausea. CT scan on the day of injury revealed no abnormality. But CT scan 12 hours following the injury showed bilateral hemorrhage of the basal ganglia. Blood pressure of the patient was within normal range and he was diagnosed as having traumatic bilateral intracerebral hematoma. Conservative treatment was carried out and the patient was discharged 7 days after injury with no neurological deficit. The mechanism of traumatic hemorrhage of the basal ganglia has not been clear. In case #1, diffuse axonal injury (DAI) may have played an important role in the bilateral hemorrhage. But in case #2, non-DAI factor such as vasoparalysis syndrome may have existed.(ABSTRACT TRUNCATED AT 250 WORDS)

Development of Delayed Posttraumatic Acute Subdural Hematoma.

Prior studies have shown that most patients with mild traumatic brain injury or negative computed tomography (CT) scans of the head rarely decline or require neurosurgical interventions. One common reason for a delayed decline is an intracranial hemorrhage that presents within 24-48 hours. This is typically seen in elderly patients and/or patients on antiplatelet or anticoagulation agents. We describe a case of a delayed subdural hemorrhage presenting in a young adult not on any antiplatelet or anticoagulation therapy. A 19-year-old male presented to the emergency department after being involved in a motor vehicle accident. He had a Glasgow Coma Scale of 15, and an initial CT was negative for any intracranial hemorrhage or pathology, so he was then admitted to the intensive care unit for further care. The patient received 1 dose of aspirin 325 mg the following day for treatment of blunt cerebrovascular injury. Six hours later he reported a severe headache and had an episode of emesis with a subsequent rapid neurologic decline. Repeat CT showed an acute right subdural hematoma, and he underwent an emergent right decompressive hemicraniectomy. In rare cases, patients with negative initial head CT scans neurologically deteriorate as a result of a delayed acute subdural hematoma. We present an unusual case of a young patient on no medications with no CT findings of an intracranial injury who neurologically declined due to a delayed acute subdural hematoma.

Acute subdural hematoma and diffuse axonal injury in fatal road traffic accident victims: a clinico-pathological study of 15 patients.

Although acute subdural hematoma (ASDH) and diffuse axonal injury (DAI) are commonly associated in victims of head injury due to road traffic accidents, there are only two clinico-pathological studies of this association. We report a clinical and pathological study of 15 patients with ASDH associated with DAI. The patients were victims of road traffic accidents and were randomly chosen. The state of consciousness on hospital admission was evaluated by the Glasgow coma scale. For the identification of axons the histological sections of the brain were stained with anti-neurofilament proteins. Twelve of the 15 patients were admitted to hospital in a state of coma; in three patients, the level of consciousness was not evaluated, as they died before hospital admission. The poorer prognosis in patients with ASDH who lapse into coma immediately after sustaining a head injury, as described by several authors, can be explained by the almost constant association between ASDH and DAI in victims of fatal road traffic accidents.

Cerebral contusion

Multiple petechial hemorrhages Numerous small contusions from broken capillaries that occur in grey matter under the cortex are called multiple petechial hemorrhages or multifocal hemorrhagic contusion. Caused by shearing injuries at the time of impact, these contusions occur especially at the junction between grey and white matter and in the upper brain stem, basal ganglia, thalamus and areas near the third ventricle. The hemorrhages can occur as the result of brain herniation, which can cause arteries to tear and bleed. A type of diffuse brain injury, multiple petechial hemorrhages are not always visible using current imaging techniques like CT and MRI scans. This may be the case even if the injury is quite severe, though these may show up days after the injury. Hemorrhages may be larger than in normal contusions if the injury is quite severe. This type of injury has a poor prognosis if the patient is comatose, even with no apparent causes for the coma. Treatment

[Acute subdural hematoma caused by mild head trauma in the aged].

We encountered 8 cases of acute subdural hematoma caused by mild head trauma in the aged. In this report, these cases were analyzed, taking into consideration clinical symptoms, CT scan, operative findings and outcome. The age ranged from 70 to 92 years (mean age of 79.7 years). 4 patients were male and 4 female. Head trauma was caused by falls in 4 patients, but in the other 4 patients the causes were unknown. Initial symptoms were headache, nausea and vomiting in 5 patients and mild disturbance of consciousness with lucid intervals in 3 patients. Seven patients had more than 100 on JCS and less than 9 on GCS on admission. Small craniotomy (HITT) was performed in 4 patients. Large craniotomy was performed in 2 patients, and decompressive craniectomy was carried out in 2 patients. The bleeding focus came from the cortical artery of the middle cerebral artery in 4 patients, cerebral contusion in 2 patients, and was unknown in 2 patients for HITT. CT scan on admission showed mixed density area of acute subdural hematoma in all of the patients, and intraventricular hemorrhage, intracerebral hemorrhage and subarachnoid hemorrhage in 3 patients. CT scan after operation revealed a new area of cerebral contusion in 3 patients, delayed traumatic intracerebral hematoma (DTICH) in 2 patients, and hypertensive intracerebral hemorrhage in 1 patient. Two patients recovered to good and fair without general complication. But the outcome in 5 patients with general complication was poor for 3 patients and fatal for 2 patients. In conclusion, large craniotomy is recommended because of bleeding from the cortical artery of the middle cerebral artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Subdural hematoma

Classification Subdural hematomas are classified as acute, subacute, or chronic, depending on the speed of their onset. Acute bleeds often develop after high-speed acceleration or deceleration injuries. They are most severe if associated with cerebral contusions. Though much faster than chronic subdural bleeds, acute subdural bleeding is usually venous and therefore slower than the arterial bleeding of an epidural hemorrhage. Acute subdural hematomas due to trauma are the most lethal of all head injuries and have a high mortality rate if they are not rapidly treated with surgical decompression. The mortality rate is higher than that of epidural hematomas and diffuse brain injuries because the force required to cause subdural hematomas tends to cause other severe injuries as well.

Intracranial hemorrhage

Subdural hematoma Subdural hematoma occurs when there is tearing of the bridging vein between the cerebral cortex and a draining venous sinus. At times they may be caused by arterial lacerations on the brain surface. Acute subdural hematoma are usually associated with cerebral cortex injury as well and hence the prognosis is not as good as extra dural hematoma. Clinical features depend on the site of injury and severity of injury. Patients may have a history of loss of consciousness but they recover and do not relapse. Clinical onset occurs over hours. A crescent shaped hemorrhage compressing the brain that does cross suture lines will be noted on CT of the head. Craniotomy and surgical evacuation is required if there is significant pressure effect on the brain. Complications include focal neurologic deficits depending on the site of hematoma and brain injury, increased intracranial pressure leading to herniation of brain and ischemia due to reduced blood supply and seizures.

[Traumatic subarachnoid hemorrhage: a prospective study of 58 cases].

We evaluated the prognostic factors in traumatic subarachnoid hemorrhage (tSAH). This study was conducted with 58 patients (44 males, 14 females; mean age 39.2; range 17 to 79 years) with tSAH, between 2001 and 2003. The patients who were admitted to the hospital within in the first 6 hours of head injury were included, whereas patients with gun shot wounds, multiple injured patients and postoperative patients were excluded. Fifty-eight patients with tSAH were prospectively followed. The neurological status of the patients and the outcomes were evaluated using Glasgow Coma Scale (GCS) and Glasgow Outcome Scale (GOS), respectively and computed tomography (CT) examinations were done according to the grading criteria by Hijdra and Fisher. The etiology of tSAH included traffic accidents (73%), falls (20%) and others (7%). The GCS scores of patients at admission were mild (9%), moderate (39%) and severe (52%). In the CT scans, the amount and distribution of bleeding was grade 1 (small SAH) in 21 patients, grade 2 (moderate SAH) in 17 patients, and grade 3 (extensive SAH) in 20 patients according to Hijdra grading system and according to Fisher's criteria. The thickness of blood layer was grade 1 (no blood) in 6 patients, grade 2 (bleeding layer less than 1 mm) in 21 patients, grade 3 (bleeding layer more than 1 mm) in 15 patients and grade 4 (ventricular bleeding) in 16 patients. Neurological outcomes of patients were favorable (good recovery or moderate disability) in 59%, and unfavorable (severe disability, persistent vegetative state or death) in 41% according to GOS. We have found in our series that the prognosis was poor in patients with poor admission scores of GCS, cysternal or fissural hemorrhage, tSAH with cerebral contusion or acute subdural hematoma, higher than 13 points according to Hidjra's classification and patients of grade 3 or 4 in Fisher's criteria.

Blunt trauma

Most patients with more severe traumatic brain injury have of a combination of intracranial injuries, which can include diffuse axonal injury, cerebral contusions, and intracranial bleeding, including subarachnoid hemorrhage, subdural hematoma, epidural hematoma, and intraparenchymal hemorrhage. The recovery of brain function following a traumatic accident is highly variable and depends upon the specific intracranial injuries that occur, however there is significant correlation between the severity of the initial insult as well as the level of neurologic function during the initial assessment and the level of lasting neurologic deficits. Initial treatment may be targeted at reducing the intracranial pressure if there is concern for swelling or bleeding within this skull, which may require surgery such as a hemicraniectomy, in which part of the skull is removed. Blunt trauma to extremities

[Surgical Treatment for Traumatic Acute Subdural Hemorrhage in the Posterior Cranial Fossa:Three Cases Reports and Review of the Literature].

Acute subdural hemorrhage(ASDH)in the posterior cranial fossa is rare. Extremely unfavorable outcomes are reported among cases accompanied by supratentorial hematoma, brainstem contusion, or intracerebellar contusion. We report three cases surgically evacuated several times for traumatic ASDH in the posterior cranial fossa simultaneously accompanied by supratentorial hematomas. In our three presented cases, the mean age was 72.3 years, and all patients were male. The mechanisms of injury included traffic accidents in two cases and fall in one. The median Glasgow Coma Scale score on admission was 6. On admission, the patients had traumatic ASDH in the posterior cranial fossa accompanied by supratentorial hematoma, so they first underwent external decompression or ICP sensor insertion for the supratentorial lesions. However, after their first surgery, all patients developed upward herniation, and subsequently underwent suboccipital craniotomy and evacuation of hematomas. Glasgow Outcome Scales were death in one case, persistent vegetable state in one case, and severe disability in one case. The patients with ASDH in the posterior cranial fossa accompanied by supratentorial hematoma should immediately undergo suboccipital craniotomy and supratentorial decompression simultaneously when the hematomas compress the brainstem and upward herniation develops.

A case of traumatic hematoma in the basal ganglia that showed deterioration after arrival at the hospital.

A case of traumatic hematoma in the basal ganglia that showed deterioration after arrival at the hospital was reported. A 65-year-old man crashed into the wall while riding a motorcycle. His Glasgow coma scale was E3V4M6 and showed retrograde amnesia and slight right motor weakness. Because head CT in the secondary trauma survey showed subarachnoid hemorrhage in the right Sylvian fissure and multiple gliding contusions in the left frontal and parietal lobe, he was entered into the intensive care unit for diagnosis of diffuse brain injury. He showed complete muscle weakness of left upper and lower limbs 5 h after the accident. Head CT newly showed hematoma, 2 cm in diameter, in the right basal ganglia. The patient vomited following the CT scan, and so his consciousness suddenly deteriorated into a stupor. We performed head CT again. The hematoma had enlarged to 5 cm at the same lesion and partially expanded into midbrain. The patient died on the 13th day of trauma. Based on retrospective interpretation, we conclude that clinical examinations, follow-up CT scans and blood examinations should be performed frequently as part of ICU management for all TBI patients in the early phase after trauma.

List of MeSH codes (C10)

– craniocerebral trauma – brain injuries – brain concussion – post-concussion syndrome – brain hemorrhage, traumatic – brain stem hemorrhage, traumatic – cerebral hemorrhage, traumatic – brain injury, chronic – diffuse axonal injury – epilepsy, post-traumatic – pneumocephalus – shaken baby syndrome – cerebrospinal fluid otorrhea – cerebrospinal fluid rhinorrhea – coma, post-head injury – cranial nerve injuries – abducens nerve injury – facial nerve injuries – optic nerve injuries – head injuries, closed – brain concussion – post-concussion syndrome – head injuries, penetrating – intracranial hemorrhage, traumatic – brain hemorrhage, traumatic – brain stem hemorrhage, traumatic – cerebral hemorrhage, traumatic – hematoma, epidural, cranial – hematoma, subdural – hematoma, subdural, acute – hematoma, subdural, chronic – hematoma, subdural, intracranial – subarachnoid hemorrhage, traumatic – skull fractures

Subdural hematoma

Prognosis Acute subdural hematomas have one of the highest mortality rates of all head injuries, with 50 to 90 percent of cases resulting in death. About 20 to 30 percent of patients recover brain function. See also Concussion Diffuse axonal injury Extra-axial hemorrhage Intra-axial hemorrhage References External links Imaging and Mechanism of Subdural Hematoma - MedPix Neurotrauma Cerebrovascular diseases zh:硬膜下血肿

List of MeSH codes (C21)

– trauma, nervous system – cerebrovascular trauma – carotid artery injuries – carotid artery, internal, dissection – carotid-cavernous sinus fistula – vertebral artery dissection – craniocerebral trauma – brain injuries – brain concussion – post-concussion syndrome – brain hemorrhage, traumatic – brain stem hemorrhage, traumatic – cerebral hemorrhage, traumatic – brain injury, chronic – diffuse axonal injury – epilepsy, post-traumatic – pneumocephalus – shaken baby syndrome – cerebrospinal fluid otorrhea – cerebrospinal fluid rhinorrhea – coma, post-head injury – cranial nerve injuries – abducens nerve injury – facial nerve injuries – optic nerve injuries – head injuries, closed – head injuries, penetrating – intracranial hemorrhage, traumatic – brain hemorrhage, traumatic – brain stem hemorrhage, traumatic – cerebral hemorrhage, traumatic – hematoma, epidural, cranial – hematoma, subdural – hematoma, subdural, acute

InternalMed_Harrison

Acute Subdural Hematoma (Fig. 457e-3) Direct cranial trauma may be minor and is not required for acute subdural hemorrhage to occur, especially in the elderly and those taking anticoagulant medications. Acceleration forces alone, as from whiplash, are sometimes sufficient to produce subdural hematoma. Up to one-third of patients have a lucid interval lasting minutes to hours before coma supervenes, but most are drowsy or comatose from the moment of injury. A unilateral headache and slightly enlarged pupil on the side of the hematoma are frequently, but not invariably, present. Stupor or coma, hemiparesis, and unilateral pupillary enlargement are signs of larger hematomas. In an acutely deteriorating patient, burr (drainage) holes or an emergency craniotomy are required. Small subdural hematomas may be asymptomatic and usually do not require evacuation if they do not enlarge.

Early computed tomography for acute post-traumatic diffuse axonal injury: a systematic review.

Diffuse axonal injury (DAI) is the rupture of multiple axons due to acceleration and deceleration forces during a closed head injury. Most traumatic brain injuries (TBI) have some degree of DAI, especially severe TBI. Computed tomography (CT) remains the first imaging test performed in the acute phase of TBI, but has low sensitivity for detecting DAI, since DAI is a cellular lesion. The aim of this study is to search in the literature for CT signs, in the first 24 h after TBI, that may help to differentiate patients in groups with a better versus worst prognosis. We searched for primary scientific articles in the PubMed database, in English, indexed since January 1st, 2000. Five articles were selected for review. In the DAI group, traffic accidents accounted 70% of the cases, 79% were male, and the mean age was 41 years. There was an association between DAI and intraventricular hemorrhage (IVH) and traumatic subarachnoid hemorrhage (tSAH); an association between the IVH grade and number of corpus callosum lesions; and an association between blood in the interpeduncular cisterns (IPC) and brainstem lesions. In closed TBI with no tSAH, severe DAI is unlikely. Similarly, in the absence of IVH, any DAI is unlikely. If there is IVH, patients generally are clinically worse; and the more ventricles affected, the worse the prognosis.

[Rapid resolution of acute subdural hematoma; report of two cases].

We reported two cases of rapid resolution of acute subdural hematoma. Case 1, a 21-year-old female, sustained head trauma and became unconscious for about 15 min. Probably she was suffering from posttraumatic amnesia for about 1 day. On admission J.C.S and G.C.S were 20 and 9 (2 + 2 + 5) points, respectively. Neurological examination showed no abnormalities. An initial computed tomography (CT) scan taken 2 hours after the injury showed a high dense subdural hematoma on the left cerebral hemisphere and hemispheric swelling. She was conservatively treated. A follow up CT scan taken 8 hours after the injury disclosed rapid disappearance of the hematoma and cerebral swelling. Case 2a 23-year-old male, sustained head trauma and became unconscious for about 30 min. On admission J.C.S and G.C.S were 1 and 14 (4 + 4 + 6) points, respectively, and slight right hemiparesis was noted. An initial CT scan taken 2 hours after the injury showed subdural hematoma of the left cerebral hemisphere and hemispheric swelling. He was conservatively treated. A follow up CT scan taken 24 hours after the injury revealed almost complete disappearance of the subdural hematoma and cerebral swelling. It was suggested that the rapid resolution of acute subdural hematoma was attributable to redistribution due to decrease of ICP, and washing out by cerebrospinal fluid.

[MRI findings of closed head injury in children; with special reference to the effect of central shearing force].

It is considered that shearing effect as introduced by Holbourn may produce central concussion, diffuse brain swelling and diffuse axonal injury according to its grade of force. MRI was performed in 38 children who had been admitted to our hospital during the previous 1 year for the treatment of closed head injury of varying severity. In 8 out of 38 cases, abnormal high signal intensity was observed in the medial and para-medial brain parenchyma on MRI. All of these 8 cases suffered from head trauma caused by motor vehicle accidents. They included 2 cases of cerebral concussion, 1 of diffuse brain swelling, and 5 cases of diffuse axonal injury. In 2 cases of cerebral concussion, MRI (T2 weighted) revealed only localized high intensity in the corpus callosum, while CT showed normal and subarachnoid hemorrhage only at the interposium. These two children had been unconscious for periods of 20 to 30 minutes. In one case of diffuse brain swelling, MRI (T2W) showed a slightly obscure border between gray and white matter due to generally increased intensity. In 5 cases of diffuse axonal injury, most of these cases manifested lesions at the corpus callosum, deep white matter, periventricular gray matter, pons, midbrain and the cerebellum as demonstrated by high signal intensity on MRI (T2W) while CT in the acute stage showed small hemorrhage at the corpus callosum, corticomedullary junction and mid-brain and in the ventricles. Among these, two cases also demonstrated subdural hematoma and cortical contusional hemorrhage. At 3-4 weeks after injury, the area of high intensity previously demonstrated in the deep white matter and the corpus callosum on MRI (T2W) was reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

Postraumatic intracranial hematomas in infancy. a 16-year experience.

The objective of this study is to analyze some of the epidemiological aspects in patients with post-traumatic intracranial hematomas (post-traumatic ICH) in infancy. These patients were treated at the Hospital Infantil Municipal de Córdoba, Argentina, between April 1980 and April 1996. A retrospective descriptive analysis was conducted on the 113 case histories of children with post-traumatic ICH, all of whom required surgical intervention during this period. Relevant information such as age, sex, mechanism of injury causing craniocerebral trauma (CCT), and data on clinical presentation on admission, diagnosis, morbidity and mortality rates were collected. The series revealed a greater incidence of post-traumatic ICH in boys (73.5%), whose average age was 6 years 5 months +/- 4 years 10 months (range 1 day to 15 years). Fifty-three percent of the girls suffered post-traumatic ICH before the age of 3, while 54% of the children were 7 years of age or older (P<0.05). Falls were the most frequent mechanism of injury causing CCT (36.3%), followed by vehicle accidents (33.6%) and unknown causes (15.9%), the latter mainly in children under 3 years old (31%). The most frequent symptoms were vomiting (58.6%), loss of consciousness (47.1%) and headaches (24.1%). Of all these children, 93.8% presented signs and symptoms at the time of hospital admission, alterations in the level of consciousness (66%), vomiting (47.2%) and headaches (26.4%) being among the most frequent. The hemorrhagic complications observed in the 113 patients took the form of extradural hematomas (EDH) in 75 (66.4%), of subdural hematomas (SDH) in 35 (31.0%), of hemorrhagic contusions (Hc) in 19 (16.8%), and of intracerebral hematomas (Ich) in 11 (9.7%). In 13 patients the site of the hematoma was the posterior cranial fossa (11.5%), and 22.1% of patients presented more than one type of hemorrhagic complication. Morbidity rates were 9.7% and mortality rates 17.7%.

[A postmortem view on "pure" subdural hemorrhages in infants and toddlers].

In the last years, the discussion concerning the causes of infantile subdural hemorrhages became controversial. Many authors still suppose that child abuse is the predominant cause of such cases. On the other hand, reports presenting series of accidental cases were published, and the fear of an overdiagnosis of the shaken baby syndrome has been expressed. Our autopsy material concerning all lethal head injuries of infants and toddlers from 2 decades was reviewed. 17 of these 64 cases were characterized by the following: history of no trauma or only an insignificant event; children found dead or apnoic or in coma; no skull fractures; no focal brain injury; ruptures of several bridging veins but only minimal subdural bleeding. 11 victims were infants (1st year of life) and either 3 were 2 years resp. 3 - 6 years old; 50 % off all lethal head injuries of infants were of this type, while only 25 % resp. 10 % of the following age groups. None of these 17 cases was a result of a minor accident witnessed by unrelated persons. Abuse could be ascertained with a high degree of probability in most cases and remained quite likely in the others. Two different types of subdural hemorrhages should be kept from another: a) patients suffering a moderate head injury from a minor accident which results in a subdural bleeding (from a small intracranial lesion) often do not deteriorate soon after the impact, develop a hemorrhage of significant volume, respond well to therapy and have a good prognosis. b) cases with a history of no or only of an insignificant trauma, infants dead or nearly dead on clinical presentation, often a poor outcome in cases of survival. There is typically no significant subdural bleeding despite multiple bridging vein ruptures in the majority of these cases: the subdural hemorrhage is here only a visible sign of a much more serious and general cerebral alteration, resulting in a rapid increase of intracranial pressure (often complicated by respiratory arrest) which prevents a signifant bleeding into the subdural space. This combination of findings is typically found in victims of massive events (car occupants in high-velocity crashes) and not compatible with a supposition of a minor fall causing this.

Acute interhemispheric subdural hematomas. Report of nine cases.

Nine male patients with acute interhemispheric subdural hematoma (ISH) are presented. The etiologic factor was trauma for all patients (traffic accident and falling down). The young adult cases and one child had bad prognosis due to severe clinical findings and high mortality. The asymptomatic patients were treated conservatively. In this report, we discussed etiologic factors, presentation of age groups, whether an ISH progresses to a chronic convexity subdural hematoma (SH), and real mortality rates for ISH with relevant literature knowledge. As a result, ISHs can present in all age groups including shaken babies, severely injured young adults as well as low velocity trauma striken elderly patients (especially those under anticoagulant medication). We believe that an acute ISH does not change to chronic convexity SH; in fact they present as simultaneous acute thin convexity SH and acute ISH. It is also concluded that in contrast to previous literature ISH and acute SH patients of similar neurological status have similar mortality rates.

[Acute traumatic subdural haematomas: study of 110 cases].

We report a series of 110 patients with acute traumatic subdural hematoma (ASDH) admitted at HBDF emergency within 1994 (January 1st to December 1st). All patients were treated according to the same protocol. There was a predominance of males (79%), with ages ranging from 14 to 70, being car accidents (20%) and car-pedestrian accidents (34%) the most frequent causes. The majority of patients (85.7%) was admitted in very serious condition, with a score of 8 points on the Glasgow Coma Scale (GCS) or lesser, which directly influenced the mortality rates. CT scan was the diagnostic procedure of choice, and it showed contusion and brain swelling to be the most frequent associated intracranial lesions. Surgery was carried out in 45.1% of cases and, in most instances, through an ample fronto-temporo-parietal craniotomy, with hematoma drainage and dural reconstitution. In 54.9% of cases, clinical conditions did not allow surgery and in this group, 69.6%.

Contrecoup Brain Injury -- Differential Diagnosis

The main differential for contrecoup injury is the condition of diffuse axonal injury (DAI). In DAI, petechial hemorrhages forms at the gray-white matter junction, corpus callosum, and brainstem. It is the result of traumatic acceleration/deceleration or rotational injuries, not attributed to a direct impact to the skull. It is a frequent cause of persistent vegetative state in patients. [20] [21]

[Traumatic hemorrhage in the basal ganglia in the child. Five cases].

Traumatic hemorrhages in the basal ganglia were seen in five children. The CT findings and the characteristics of these injuries were discussed. All of children were injured in car accidents. They ranged in age from 3 to 13 years. The patients comprised 3 boys and 2 girls. On admission, case 1 was conscious and case 2 was in a stupor. Case 1 and 2 were mild cases in which spotty hematomas were seen in the ganglionic region. They recovered fully. Case 3-5 were severe cases in which massive hematomas were seen in the ganglionic region. On admission, their consciousness ranged from stupor to coma. We performed operations on two of them but their recoveries were unsatisfactory. Their results were as follows. One had residual hemiparesis and dysarthria, one experienced tetraparesis and dysarthria and the last went from coma to a vegetative state. Concerning the directions of the impacts, 4 were hit in the frontal region or face and the last one received blows on the occipital region. Skull fractures were seen in two cases. Mandibula and clavicula fractures were seen in the other two cases. Only one child had no fractures. We conclude that pediatric traumatic hemorrhages in the basal ganglia are induced by severe impact on the frontal or occipital regions. The size of hematomas in this injury is spotty or massive. The massive type has a poor prognosis. On the other hand, the spotty type's prognosis is good. We speculate that impact to the head causes a shear strain in the ganglionic region. At that time, vessels in the area are injured.

[A case of acute subdural hematoma in the posterior fossa with idiopathic thrombocytopenic purpura].

Intracranial bleeding is one of fatal complications in idiopathic thrombocytopenic purpura although its reported incidence is low. A case of spontaneous acute subdural hematoma complicated with idiopathic thrombocytopenic purpura was reported. He was hospitalized complaining of sudden onset of headache and nasal bleeding without neurological deficit. CT scan revealed subdural hematoma in the posterior fossa especially below the tentorium cerebelli. Further hematological examination proved very low platelet count (1,000/mm3) and antiplatelet antibody in confirmation of a diagnosis of idiopathic thrombocytopenic purpura. As his neurological status was good, he was treated medically. His symptoms and platelet count improved gradually with corticosteroid therapy. Reviewing the literature, acute subdural hematoma with idiopathic thrombocytopenic purpura was quite rare and only three cases reported.