Acute epidural hematoma developing during twist-drill craniostomy: a complication of percutaneous subdural tapping for the treatment of chronic subdural hematoma

BACKGROUND

This case illustrates that although percutaneous subdural tapping for patients with chronic subdural hematoma (CSDH) is successful and minimally invasive, it can be complicated by acute epidural hematoma.

CASE PRESENTATION

A 62-year-old woman presented with headache two months after minor head trauma. Computed tomography (CT) scanning revealed CSDH with mixed density on the right side. Prior to percutaneous subdural tapping, twist-drill craniostomy was performed at the parietal tuber. When the drill-needle reached the dura mater, the patient began to complain of headache, which was followed by altered consciousness. CT scanning disclosed acute epidural hematoma abutting the CSDH; both hematomas were evacuated by emergency craniotomy. At surgery, no definite bleeding source was identified apart from oozing on the dura mater.

CONCLUSION

Hemorrhagic complications after percutaneous subdural tapping are rare. The formation of acute epidural hematoma during twist-drill craniostomy has not been reported in the literature. This complication can occur when the blunt tip of the drill-needle remains on the dura mater without penetrating into the subdural hematoma cavity.     

Single burr hole surgery for acute spontaneous subdural hematoma in the aged: patient reports of three cases

The method of treatment for acute spontaneous subdural hematoma in aged patients is controversial. Three cases of acute spontaneous subdural hematoma in aged patients, treated by single burr hole drainage without irrigation, were reported. The first case, an 80-year-old male was admitted with complaints of headache and stupor without any history of head trauma. CT revealed a left subdural hematoma with mixed density. Intractable facial convulsion occurred three days after admission. Single burr hole drainage was performed to remove the hematoma, and facial convulsion disappeared one week after the surgery. The second case, a 70-year-old male was admitted with complaints of consciousness disturbance without any history of head trauma. CT showed a right subdural hematoma with mixed density. The next day, he recovered consciousness and CT demonstrated shrinkage of the hematoma. However, his consciousness deteriorated again 11 days after admission, and CT revealed progression of the hematoma. We performed single burr hole drainage, and the next day, his neurological condition recovered. The third case, an 84-year-old female was admitted with complaints of consciousness disturbance without any history of head trauma. CT revealed a left subdural hematoma with mixed density. Single burr hole drainage was performed to remove the hematoma. She recovered completely and was discharged and return home 1 month after the surgery. Single burr hole drainage is less invasive than craniotomy. Our three cases indicate that this method may be one of the best methods for aged patients with acute spontaneous subdural hematoma which manifests mixed density in CT.     

Two cases of impending herniation due to multiple traumatic acute subdural hematomas: combination of burr hole evacuation and craniotomy

A contralateral extra-axial hematoma sometimes occurs during an operation on an acute subdural hematoma and may become fatal. Using a combined procedure of burr hole evacuation and craniotomy, we treated 2 cases of multiple traumatic acute subdural hematomas. Our policy for such cases is first to perform a burr hole evacuation for the acute subdural hematoma in the emergency room, while simultaneously preparing the operation room for a possible further operation. Next, we perform computed tomography (CT) of the brain. If the evacuation does not provide enough decompression, we either carry out a craniotomy at the same site, or, we observe the patient without resorting to craniotomy. However, if the patient's condition deteriorates, burr hole evacuation is repeated and/or craniotomy is carried out as soon as possible on the lesion at the already prepared operation room. Both of our patients received craniotomy for another subdural hematoma after the burr hole evacuation. Though his intracranial pressure was well managed during the acute stage, one of the patients died 21 days after the trauma due to an extensive brain infarction caused by vasospasm. The other regained consciousness and was able to walk 5 months after the trauma in spite of cerebral infarction from vasospasm. The possible mechanism of vasospasm in severe head injury is also discussed.     

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)     

Acute epidural-like appearance of an encapsulated solid non-organized chronic subdural hematoma

We report the exceptional case of an encapsulated solid non-organized chronic subdural hematoma (SDH) in a 67-year-old woman that was admitted with acute hemiplegia followed by rapid deterioration in consciousness 5 months after a minor head trauma. Computed tomography (CT) showed an extracerebral biconvex shaped hyperdense mass that led to the misdiagnosis of an acute epidural hematoma. Urgent craniotomy revealed an encapsulated mass filled with solid fresh clot in the subdural space. Complete evacuation of this SDH, including both its inner and outer membranes, was achieved, and the patient recovered successfully. Histological analysis confirmed that the content of the hematoma corresponded to a newly formed clot that was enclosed between an inner membrane, composed of two collagen layers, and an outer membrane with a three layered structure. Chronic SDH may seldom present as an encapsulated solid non-organized lesion that consists of a fibrous capsule enclosing a fresh clot and lacking the thick fibrous septations that typically connect the inner and outer membranes of organized chronic SDH. This entity mimics the clinical course and radiological appearance of acute epidural hematomas and should be considered in the differential diagnosis of extracerebral hyperdense biconvex shaped lesions.     

Acute subdural hematoma after intra-arterial thrombolysis for acute ischemic stroke--case report

A 79-year-old man with a cardiac pacemaker for bradycardia fell down and presented with sudden onset of right hemiplegia and aphasia. Initial computed tomography (CT) showed no cerebral infarction but angiography revealed occlusion of the left middle cerebral artery (MCA). Local intra-arterial thrombolysis with tissue plasminogen activator (tPA; tisokinase, 1,600,000 units) was performed 3 hours after the onset, and the MCA was partially recanalized. Further administration of tPA was suspended because of nosebleed. However, the patient's neurological findings did not improve. His consciousness gradually deteriorated to coma and quadriplegia with dilation of the left pupil 2.5 hours after thrombolysis. CT disclosed marked mass effect with a left acute subdural hematoma and a small intracerebral hematoma in the left frontal lobe. He underwent urgent craniotomy and removal of the subdural hematoma. The subdural hematoma originated in a frontal cerebral contusion. He died of severe brain edema 2 days after surgery. Acute subdural hematoma is a very rare complication of intra-arterial thrombolysis. Presumably he had suffered head trauma at the first onset. Evidence of head trauma should be considered a contraindication for the use of thrombolytic agents in a patient with acute stroke.     

Acute subdural hematoma due to minor head trauma in patients with a lumboperitoneal shunt

The cases of four patients treated with a lumboperitoneal shunt in whom acute subdural hematoma occurred after minor head trauma are presented. Three of the four patients had subdural fluid collection or widening of subarachnoid space observed on computed tomography scan after placement of the lumboperitoneal shunt. We report that patients with a lumboperitoneal shunt have the potential to develop acute subdural hematoma due to minor head trauma, and discuss its mechanism.     

Acute subdural hematoma in infancy

BACKGROUND: Acute subdural hematoma in infants is distinct from that occurring in older children or adults because of differences in mechanism, injury thresholds, and the frequency with which the question of nonaccidental injury is encountered. The purpose of this study is to analyze the clinical characteristics of acute subdural hematoma in infancy, to discover the common patterns of this trauma, and to outline the management principles within this group. METHODS: Medical records and films of 21 cases of infantile acute subdural hematoma were reviewed retrospectively. Diagnosis was made by computed tomography or magnetic resonance imaging. Medical records were reviewed for comparison of age, gender, cause of injury, clinical presentation, surgical management, and outcome. RESULTS: Twenty-one infants (9 girls and 12 boys) were identified with acute subdural hematoma, with ages ranging from 6 days to 12 months. The most common cause of injury was shaken baby syndrome. The most common clinical presentations were seizure, retinal hemorrhage, and consciousness disturbance. Eight patients with large subdural hematomas underwent craniotomy and evacuation of the blood clot. None of these patients developed chronic subdural hematoma. Thirteen patients with smaller subdural hematomas were treated conservatively. Among these patients, 11 developed chronic subdural hematomas 15 to 80 days (mean = 28 days) after the acute subdural hematomas. All patients with chronic subdural hematomas underwent burr hole and external drainage of the subdural hematoma. At follow-up, 13 (62%) had good recovery, 4 (19%) had moderate disability, 3 (14%) had severe disability, and 1 (5%) died. Based on GCS on admission, one (5%) had mild (GCS 13-15), 12 (57%) had moderate (GCS 9-12), and 8 (38%) had severe (GCS 8 or under) head injury. Good recovery was found in 100% (1/1), 75% (8/12), and 50% (4/8) of the patients with mild, moderate, and severe head injury, respectively. Sixty-three percent (5/8) of those patients undergoing operation for acute subdural hematomas and 62% (8/13) of those patients treated conservatively had good outcomes. CONCLUSIONS: Infantile acute subdural hematoma if treated conservatively or neglected, is an important cause of infantile chronic subdural hematoma. Early recognition and suitable treatment may improve the outcome of this injury. If treatment is delayed or the condition is undiagnosed, acute subdural hematoma may cause severe morbidity or even fatality.     

Ruptured traumatic aneurysm after trivial injury mimicking acute spontaneous subdural hematoma--case report-

A 75-year-old man suffered acute subdural hematoma shortly after trivial head trauma. Thirteen hours after a trivial brow to the occipital region, caused by contact with a mat, he suddenly deteriorated to the level of a Glasgow Coma Scale score of 6. Computed tomography demonstrated an acute subdural hematoma on the left and angiography revealed an aneurysm of the distal middle cerebral artery. An emergent craniotomy disclosed no skull fracture and exposed a thick subdural hematoma with no brain contusions. After evacuation of the hematoma, an aneurysm was found on the distal portion of posterior temporal artery, which was compatible with the angiographical findings. The neck of aneurysm was so fragile that neck clipping could not be successfully performed. Therefore, the aneurysm was extirpated, and the bleeding site coagulated with oxidized cellulose reinforcement. Histological examination of the aneurysm indicated a pseudoaneurysm during the early phase of clot formation. The acute subdural hematoma resulted from rupture of this pseudoaneurysm which was formed shortly after the minor head trauma. Rupture of a pseudoaneurysm caused by trivial trauma might be one of the origins for so-called acute "spontaneous" subdural hematoma.     

Acute subdural hematoma after lumboperitoneal shunt placement in patients with normal pressure hydrocephalus

Acute subdural hematoma (SDH) is a rare but disastrous complication after lumboperitoneal shunt placement. Four of 206 adult patients with normal pressure hydrocephalus (1.9%) who underwent lumboperitoneal shunt placement suffered acute SDH following head trauma. The interval between shunt placement and acute SDH was one month to 7 years. Two patients had subdural effusion on computed tomography (CT) at 2- and 6-month follow up. All four patients required assistance in their daily activities before acute SDH onset. The traumatic event was a fall. On admission, CT revealed a large SDH that required surgical removal in two patients, of whom one had manifested subdural effusion after shunt placement. The other two patients had a small SDH. None of the four patients had cerebral contusions. Patients with lumboperitoneal shunts, especially those not capable of independent daily activities, are at risk for acute SDH after even minor head trauma.     

Two cases of acute idiopathic subdural hematoma with delayed intracranial hypertension

Two cases of acute idiopathic subdural hematoma with delayed intracranial hypertension were presented. The first case was a 68-year-old man admitted for vomiting following headache for eight days. There was no history of head trauma. A CT scan revealed a high-density mass that had a concave inner margin in the left temporo-parietal region with a slight midline shift. No vascular lesion was noted on the angiogram. The consciousness of the patient deteriorated suddenly on the 12th day. An operation was performed because of a marked midline shift on the CT. At operation, a subdural clot was removed. The postoperative recovery was good. The patient was discharged 7 days later without any neurological deficit. The second case was a 69-year-old man who was admitted with sudden onset of headache. There was no history of head trauma. A CT scan showed a high density mass in the right temporoparietal subdural space with a slight midline shift. The consciousness of the patient deteriorated suddenly on the 15th day. An operation was performed because of a marked midline shift on the CT. At operation, a subdural hematoma was removed. Two days later, suddenly his consciousness deteriorated. A CT scan showed his severe brain edema with a marked midline shift without increased hematoma. External decompression was performed immediately. The postoperative recovery was very good and 40 days after the second operation, the patient was discharged with no neurological deficit. The delayed intracranial hypertension appeared in these two cases about 10 days after the initial symptom. Two kinds of mechanisms are suspected: 1) swelling of the hematoma because of the adsorption of cerebrospinal fluid, 2) the occurrence of secondary brain edema. From our experience, a repeated CT scan is necessary for 2 to 3 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute spontaneous subdural hematoma of arterial origin

BACKGROUND: Acute subdural hematoma is usually associated with cerebral contusion or laceration of the bridging veins following a head injury. However, several cases of acute subdural hematoma without head injury (acute spontaneous subdural hematoma) have been reported. METHODS: Among 162 cases of acute subdural hematoma admitted to our departments between 1996 and 2003, we repoort eight cases of acute spontaneous subdural hematoma. These cases fulfilled the following criteria. 1) Head injury was either trivial or absent. 2) Neither aneurysm nor arteriovenous malformation was apparent. 3) CT scan revealed neither brain contusion nor traumatic subarachnoid hemorrhage. 4) At operation, laceration of the cortical artery was observed. In this article, we describe the clinical feature (age, sex, Glasgow Coma Scale [GCS] Score on admission, past history, CT appearance, and outcome) associated with this condition. RESULTS: Patients ranged in age from 68 to 85 years (average 74.8 years), and were comprised of 3 males and 5 females. Previous medical history included cerebral infarction in 6 of the 8 patients and myocardial infarction in 1 patient. These seven patients were taking antiplatelet manifestation. GCS on admission ranged from 4 to 13. Five of the 7 patients on antiplatelet medication had secondary insults, such as hypoxia. On CT, hematoma thickness ranged from 13.2mm to 42.5mm (average 22.6mm), and midline shift ranged from 10.0mm to 24.0mm (average 16.5mm). Neurological outcome evaluated using the Glasgow Outcome Scale was as follows, good recovery n = 2, moderate disability n = 2, severe disability n = 3, persistent vegetative state n = 1. CONCLUSION: The mechanism of acute spontaneous subdural hematoma is influenced by the presence of pre-existing cerebrovascular disease and by the use of antiplatelet agents. In such cases, the possibility of cortical arterial bleeding should be taken into account, and craniotomy should be performed.     

Successful surgical treatment of a hemophiliac infant with nontraumatic acute subdural hematoma

BACKGROUND: The moderate hemophiliacs usually have no spontaneous bleeding, but bleed after minor or major trauma. The proper management of intracranial hemorrhage in hemophiliac children is a challenge. CASE DESCRIPTION: An 18-month-old male infant with moderate hemophilia A was admitted with fever, vomiting, and hypersomnia. There was no history of trauma or seizure. The CT scans showed an acute subdural hematoma in the right temporoparietooccipital region with midline shift and a coincidental right cerebellar arachnoid cyst. After bolus factor VIII replacement, a right temporoparietal craniotomy was performed, and the subdural hematoma was evacuated. The postoperative CT scans demonstrated no hematoma. CONCLUSIONS: The possibility of intracranial hemorrhage in a moderate hemophiliac infant should be considered even if the patient has no history of trauma. The surgical treatment results in a successful outcome in hemophiliac children with subdural hematomas provided that an aggressive factor replacement therapy is initiated before surgery.     

The accuracy of near-infrared spectroscopy in detection of subdural and epidural hematomas

BACKGROUND: We evaluated the safety range of near-infrared spectroscopy (NIRS) in the management of trauma patients who had subdural or epidural hematomas in the emergency room and intensive care unit. METHODS: Thirty cases with the radiologic diagnosis of subdural and epidural hematomas were evaluated pre- and postoperatively by NIRS. The findings were analyzed by comparing the data of 30 minor head trauma patients without hematoma, which was proven by computed tomography imaging using Mann-Whitney U and McNemar tests. RESULTS: The preoperative accuracy of NIRS in detecting the hematoma existence was same as the accuracy of the radiologic imaging but the postoperative findings were not reliable. The sensitivity of the device in detecting abnormality was found to be 0.87. CONCLUSION: NIRS is a good device to predict intracranial subdural and epidural hematomas in the field and emergency units. However, it is not superior to computed tomography or magnetic resonance imaging. It is useful in emergency situations to diagnose an intracranial bleeding but NIRS is not reliable to detect either postoperative hematomas or intracranial status in patients with craniotomy.     

Infected and calcified chronic subdural hematoma presenting an attitude of acute hematoma on MRI: case report

We report a case of calcified chronic subdural hematoma with unusual magnetic resonance imaging (MRI) findings. A 50-year-old male with no marked medical history presented with fever for two weeks. Computed tomography (CT) revealed a thick, calcified subdural hematoma of low-iso mixed density. MRI showed characteristic signals of hematoma in the acute stage. Total removal of the hematoma by craniotomy was performed after rapid deterioration of consciousness. At surgery, a muddy hematoma and a small amount of pus were seen within the calcified capsule. Diagnosis of infected and calcified chronic subdural hematoma was established. His symptoms were resolved completely within the following few months. As the mechanisms of delayed signal sequence of hematoma on MRI, we speculate existence of tissue hypoxia associated with infection and paramagnetic effects of free radicals and ions associated with inflammation, necrosis and calcification.     

Early seizures after mild closed head injury.

The authors review the seizure incidence in 4232 adult patients with mild closed head injury who did not receive prophylactic anticonvulsant agents. One hundred patients (2.36%) experienced seizures within 1 week after head injury; 43 of these (1.02% of the series) had seizures within 24 hours after trauma. Most of the seizures (84%) that developed during the 1st week after injury were of the generalized tonic-clonic type. The incidence of generalized tonic-clonic seizures was higher than that of partial seizures with motor symptoms both within 24 hours (91% vs. 9%) and during the Day 2 to 7 period (79% vs. 21%). No definite intracranial pathological findings were detected by computerized tomography (CT) in 53% of patients with early posttraumatic seizures; six patients had intracranial hemorrhage without intracranial parenchymal damage (three with epidural hematoma and three with subarachnoid hemorrhage). The most common positive CT findings in the early posttraumatic-seizure group were intracerebral hemorrhage (24%), followed by acute subdural hematoma with intracerebral hemorrhage (17%). Intracerebral parenchymal damage could be identified on CT scans in 41 (48.8%) of 84 patients with generalized tonic-clonic seizures and five (31%) of 16 patients with partial seizures with motor symptoms. The intracerebral parenchymal damage was most commonly detected in the frontal lobe (21%) and the temporal lobe (19%). Seven patients with early posttraumatic seizures received emergency craniotomy to remove an intracranial hematoma (epidural in three, subdural and intracerebral in four) because the mass effect resulted in significant midline shift as seen on CT scans. This review suggests that early posttraumatic seizures after mild closed head injury have a high incidence (53%) in patients with normal CT scan findings. Although the possibility of surgically correctable intracranial hemorrhage is low (7%), the condition may be devastating if not treated properly.     

Computerized tomography findings of acute traumatic epidural hematoma

During four year period from April, 1977 to March, 1981, 53 cases with acute traumatic epidural hematoma had been encountered out of 430 acute head injured patients examined by computerized tomography (CT) within 24 hours after incurring the trauma at the Department of Neurosurgery and Critical Care Medicine of Nippon Medical School, Sendagi, Tokyo, Japan. Besides the initial CT, the authors performed contrast enhanced CT (41 cases) and serial CT scanning (31 cases). There were 49 cases of epidural hematoma existing in the supratentorial region, Two cases infratentorial region and 2 cases in the both regions. Two cases of vertex epidural hematoma had been encountered, one of them required vertical scan technique. In 22 (41%) of the 53 patients, the initial CT showed evidence of other cerebral lesions. The most frequent lesion was pneumocephalus (11 cases), 3 cases of them existed in the epidural hematoma. There were also intracerebral hematoma (6 cases), subdural hematoma (4 cases), cerebral contusion (2 cases), intraventricular hemorrhage (2 cases) and 2 cases of them demonstrated "diffuse traumatic cerebral injury" (Zimmerman, 1979). During contrast enhanced CT, 11 cases out of 41 cases indicated several enhancement pattern. There were total enhancement of epidural hematoma (2 cases), partial enhancement of hematoma (2 cases) and enhancement of internal margin of hematoma (2 cases). Serial CT scans was performed in 36 out of the 53 patients. Common findings on the serial CT scans were decreased density collection in the subdural space such as subdural effusions or chronic subdural hematomas (8 cases) and enlargement of small epidural hematomas (3 cases).(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute subdural haematoma successfully treated by percutaneous subdural tapping in an elderly patient

Summary An elderly patient suffering acute subdural haematoma associated with cerebral contusion was treated by percutaneous subdural tapping while preparing for craniotomy. Most of the subdural haematoma, though of high density on computed tomography scanning, proved to be semiliquid. Drainage of the haematoma yielded resolution of the mass effect, and was followed by a rapid improvement of consciousness. This observation suggests the significance of trial subdural tapping for the treatment of acute traumatic subdural haematoma prior to craniotomy.     

Three cases of chronic subdural hematoma developing after direct aneurysmal surgery (author's transl)

Three cases of chronic subdural hematoma developing after direct aneurysmal surgery were presented. All patients were males and heavy drinkers. There was no history of head injury after craniotomy. In two of the three cases, the angiography was performed on the 12th postoperative day. An avascular area was already revealed on the postoperative angiograms, but there were no disorders at that time. The intervals between the aneurysmal surgery and the onset of symptoms of chronic subdural hematoma ranged from about two to three months. In this report, the diagnostic criteria for the chronic subdural hematoma resulted from intracranial surgery were also discussed with a consideration on the pathogenesis of this condition.     

The influence and outcome of acute infantile intracranial hematoma with hypoxemia

Unusually broad areas of cerebral infarction were demonstrated by CT scan in three head injured infants with acute intracranial hematoma. They revealed very characteristic CT findings including contralateral hemispheric ischemic zone. Case 1 is a 5-month-old boy who had hit his head 4 days before. On admission he was semicomatose and his respiration had suffered from generalized seizures with arterial PO2 value of 43 mmHg. CT scan revealed right subdural hematoma, and bihemispheric ischemic low density was also demonstrable. Hematoma clot weighing 10 grams was removed through emergency craniotomy, followed by external decompression. There was a marked atrophic change in the right cerebral hemisphere and contralateral frontal base during the following few months, but the basal ganglionic region, brainstem and cerebellum were hardly affected. The patient developed comparatively well mentally for the next one and a half years. Case 2 was a 2-year-old boy who had a previous history of moderate head trauma 8 hours before admission. After a lucid interval, sudden epileptic attacks hospitalized him in a condition of cardiopulmonary arrest. CT scan revealed severe epidural hematoma on the patient's right cerebrum. Emergency craniotomy was performed and hematoma 95 g in weight was removed followed by decompression. Postoperative CT showed broad ipsilateral ischemic edema including the contralateral cerebral hemisphere and brainstem. One and a half years later, the patient shows decorticated posture with ataxic respiration and negative light reflexes. Case 3 was an 8-month-old boy who had fallen down and hit his head on the floor. Status epilepticus had attacked him, causing him to be admitted in a dyspneic state.(ABSTRACT TRUNCATED AT 250 WORDS)