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)     

Rapid reduction of acute subdural hematoma and redistribution of hematoma: case report

An 88-year-old woman presented with acute subdural hematoma (ASDH) which showed rapid resolution on computed tomography (CT) and magnetic resonance (MR) imaging. She was transferred to our hospital after falling out of bed. On admission, she was comatose with Japan Coma Scale score of 200 and Glasgow Coma Scale score of E1V1M2. Brain CT showed a thick left frontotemporal ASDH. Conservative treatment consisted of 200 ml of glycerol administered intravenously twice a day, and maintenance in the approximately 20 degree head-up position to reduce intracranial pressure. Three days later, her consciousness recovered to Japan Coma Scale score of 30 and Glasgow Coma Scale score of E2V4M5. CT showed obvious reduction of the hematoma without brain or scalp swelling. Spinal MR imaging detected no redistribution of hematoma to the spine. The present case illustrates that rapid spontaneous reduction of ASDH may occur by redistribution of hematoma, mainly to the supratentorial subdural space because of brain atrophy.     

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.     

Acute subdural hematoma due to near-drowning--case report

A 46-year-old male was transferred to our hospital after near-drowning when swimming. Examination found no subcutaneous hematoma or abrasion on his head. Cardiopulmonary resuscitation was started immediately. Emergent computed tomography (CT) revealed no abnormalities. The next day, his consciousness level improved and repeat CT suggested an acute spontaneous subdural hematoma in the parieto-occipital region. The acute subdural hematoma was evacuated. The source of bleeding was probably an abnormally large vein located in the center of the hematoma. The patient was discharged without neurological deficit. Repeat CT is needed even if there were no abnormality on initial CT after drowning.     

A case of posttraumatic delayed cerebral arterial spasm; case report and review of the literature on the pathogenesis]

A case of posttraumatic delayed cerebral arterial spasm is presented. A 71-year-old man was admitted to our hospital with head injury. Neurological examination on admission only revealed consciousness disturbance (Japan Coma Scale 30). CT scan 19 hours after the injury demonstrated a contusional hematoma in the right frontal lobe, faint subarachnoid hemorrhage in the left sylvian fissure and subdural hematoma in the interhemispheric fissure. His consciousness was disturbed on the 14th day. CT scan demonstrated a left subdural effusion, which was surgically evacuated. However, from the next day the patient developed left hemiparesis. Right carotid angiogram on the 17th day after the injury revealed multiple segmental arterial narrowing in the right anterior cerebral artery (ACA) and middle cerebral artery (MCA). We diagnosed a posttraumatic delayed cerebral arterial spasm. CT scan revealed low density areas in the right ACA and MCA territory. The pathogenesis of posttraumatic delayed arterial spasm is not yet well known. Now, four theories have been suggested as follows: (1) Subarachnoid hemorrhage, (2) Direct mechanical injury to the arterial wall, (3) Hypothalamus dysfunction, and (4) Disturbed autoregulation. In our case, three important factors are suggested. The first is direct injury to the artery, the second is cerebral contusion, and the third is subdural effusion.     

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 secondary to cerebrospinal fluid drainage during thoracic endovascular aortic repair (TEVAR): A case report

We report a case of acute subdural hematoma which occurred following cerebrospinal fluid (CSF) drainage during thoracic endovascular aortic repair (TEVAR) surgery. A 63-year-old woman was scheduled to receive TEVAR for thoracic-abdominal aneurysm extending from the descending aorta (T10) to 15 mm above the celiac trunk. Before the TEVAR operation, a lumbar cerebrospinal drain was inserted at L4-5. CSF pressure was maintained at 10cmH2O throughout the operation. The surgical procedure was completed uneventfully. At the end of the surgery, the attending anesthesiologist recognized an inequality in the patient's pupil size. Emergency CT scan reviewed left acute subdural hematoma. The patient underwent emergency external decompression surgery. The benefits of CSF drainage for spinal cord protection is well established, and ischemia of Adamkiewicz artery is prevented by careful control of CSF pressure. However, the use of CSF drainage has been associated with the risk of acute subdural hematoma. Careful observation for amount of CSF drainage is necessary during thoracoabdominal aortic aneurysm repair.     

Calcified chronic subdural hematoma complicated with subcortical hemorrhage: case report

The patient was a 46-year-old male, who suffered from mild head trauma in January 2002, and general convulsions with unconsciousness on February 28. Slight right hemiparesis and aphasia were presented after the epilepsy attack. CT scan revealed a large lesion of mixed density occupying the left temporal space. It showed linear high density in its medial margin and had compressed the left temporal lobe strongly, causing mid-line shift. The lesion was suspected to be a calcified chronic subdural hematoma and the patient was admitted to our hospital on February 28. The symptoms had improved the next day but they began to get worse again gradually after admission. T1-weighted MR image showed high intensity areas under the subdural hematoma, which were suspected to be subcortical hemorrhage. Six days after admission, consciousness disturbance became progressive. The calcified hematoma had not enlarged but brain edema had increased. On CT, an operation was performed and the calcified old hematoma and the new subdural hematoma surrounding it were removed. The diagnosis of organized chronic subdural hematoma was made at the time of the operation. The contents of this calcified subdural hematoma was mostly old dark-gray substance, but some fresh bleeding point was seen at the inner surface of the outer membrane. At the bottom there was a hard, calcified layer which adhered tightly to the brain. Adhesion between the inner membrane of the hematoma and brain surface which related to the subcortical hemorrhage was presented. It seemed impossible to remove the inner membrane without damaging the brain so no attempt was made to do so. The aphasia and right hemiparesis improved 3 weeks after the operation and the patient was discharged on April 4. He has no neurological deficits and is under periodic observation. A calcified chronic subdural hematoma has rarely been encountered and the etiology, imaging diagnosis, and management are unclear. We presented the interesting image findings on this case and discussed the etiology of this disease.     

Successful surgical treatment of subdural hematoma following mitral valve replacement]

A 56-year-old woman, followed after mitral commissurotomy, was admitted to the hospital because of congestive heart failure of NYHA IV. Cardiac catheterization demonstrated severe MSR and TR. MVR using a SJM prosthetic valve and TAP with DeVega's method were performed under cardiopulmonary bypass with moderate hypothermia (25 degrees C). Postoperative hemodynamic condition was good with a uneventful convalescence. But disturbance of consciousness was seen with gradual deterioration and anisocoria developed on the 4th postoperative day. CT scan revealed a subdural hematoma in the right frontal and parietal region. Irrigation of the hematoma was performed immediately by neurosurgeons. She resumed full consciousness and was discharged from the hospital without any sequelae on the 49th postoperative day. The importance of the early diagnosis and the immediate treatment for the subdural hematoma following open heart surgery was emphasized.     

One-stage operation for esophageal perforation of a thoracic aortic aneurysm

The patient was a 65-year-old man. Preoperative computed tomography showed a ruptured thoracic aortic aneurysm that formed a submucosal hematoma in the thoracic esophagus with perforation near the esophageal-cardiac junction. A one-stage operation was performed. The aortic arch and proximal descending aorta were replaced with rifampicin-soaked synthetic grafts, followed by subtotal esophagectomy with primary reconstruction using a gastric tube. His early postoperative course was uneventful, and he started oral intake on postoperative day (POD) 15; however, dysphagia occurred on POD 20, and an esophageal fistula and mediastinitis developed more than 1 month after the operation. The patient recovered from mediastinitis after 4 months of mediastinal drainage and administration of antibiotics. Thus, a one-stage operation for esophageal perforation of a ruptured thoracic aortic aneurysm with primary esophageal reconstruction is possible in selected patients. Care must be taken to avoid postoperative compression of the reconstructed esophagus by a mediastinal hematoma.     

Three cases of non-traumatic acute subdural hematoma]

The authors present three cases of non-traumatic acute subdural hematoma showing interesting clinical features and operative findings. Case 1: A-50-year-old male was admitted because of sudden headache and epileptic seizure. Computed tomographic (CT) scan showed a right thin subdural hematoma, but cerebral angiography demonstrated no pathological findings, that might cause acute subdural hematoma on the follow-up CT scans. The hematoma changed to a chronic one within only 15 days, which was proved by the operation. Case 2: A 52-year-old male was hospitalized because of loss of consciousness. CT scan revealed a right subdural hematoma without subarachnoid hemorrhage and cerebral angiography demonstrated a right middle cerebral artery aneurysm. The hematoma was surgically proved to be due to rupture of the aneurysm. Case 3: A 52-year-old male was admitted because of headache, vomiting and left motor weakness. CT scan showed a thick right subdural hematoma and right carotid angiography revealed two internal carotid artery aneurysms. It was surgically certified that the subdural hematoma was caused by a tear in a cortical artery attached to the dura, not by the rupture of the aneurysms. Clinical cause and pathogenesis of so-called "non-traumatic" or "spontaneous" acute subdural hematomas were discussed, and the importance of emergency angiography for this condition is stressed.     

Intracerebral hemorrhage immediately following the operation of chronic subdural hematoma

Complications following the operations for chronic subdural hematoma include recurrence of the hematoma, infection, seizure, and failure of the brain to expand due to cerebro-cranial disproportion. This report presents cases with intracerebral hemorrhage which is relatively rare complication. In case 1, a 35-year-old man developed status epilepticus immediately after the operation for chronic subdural hematoma. An emergency CT scan revealed acute brain swelling, and still, after the external decompressive craniotomy, CT scan showed severe brain swelling with subcortical diapedetic hemorrhage. In case 2, a 78-year-old woman whose CT scan had shown bilateral CSH and brain herniation, demonstrated intracerebral hemorrhage in the medial occipital lobe when examined post-operatively by CT scan. It is possible that the mechanisms of intracerebral bleeding following the operation for CSH are 1) diapedesis through increased permeability of parenchymal blood vessels due to the sudden increase in cerebral blood flow following the existence of longstanding extracerebral mass, and 2) hemorrhagic infarction due to recanalization of posterior cerebral artery compressed by the herniating medial temporal lobe. We should therefore avoid sudden decompression in the management of the cases which showed pre-operative consciousness disturbance or abnormal low or high density on CT scan, because these findings may be preoperative indications of brain fragility.     

Ultra rapid spontaneous resolution of acute posttraumatic subdural hematomas in patient with temporal linear fracture

Summary ¶We report a case of 57 year-old man with documented posttraumatic acute subdural hematoma and a linear temporal bone fracture. He suffered from a blunt head injury and presented with sudden loss of consciousness. Within 2 hours he became alert and oriented. Follow-up CT scan of brain 2 hours after the initial one showed resolution and redistribution of the subdural hematoma.To our knowledge, this is the first case in the literature about spontaneous resolution of an acute subdural hematoma in a patient with a linear fracture and the fastest resolution period. In this article, the authors discuss the underlying pathophysiology of this uncommon phenomenon.Published online July 23, 2003     

A pathogenesis of chronic subdural hematoma; it's relationship to subdural membrane]

Our report concerns 112 cases of chronic subdural hematoma (CSH). M:F ratio is 3.5:1. (Fig. 1). The etiology of CSH is as follows; mild head injury (71 pts.), post-craniotomy (3 pts.), post-V-P shunt (1 pt.) and unknown (37 pts.). All patients are diagnosed by CT scan. Twenty patients were followed up after the subdural space was expressed as low density on CT (Fig.2). 14 of these were found to have extremely thin subdural fluid collection without compression of the brain. Cisternography by using radioisotope and/or metrizamide was carried out in seven patients in whom the subdural fluid collection was found on CT, and in five of whom the dye flowing into the subdural space was retained for 24-48 hours (Fig. 3 a). For treatment, burr holes and irrigation of the hematoma was carried out and then a drain was inserted into the subdural space. The inner membrane of the chronic subdural hematoma was looked at in 19 patients during surgery. All but one showed the inner membrane totally covering the brain surface. However, in one patient the inner membrane didn't entirely cover the brain surface, suggesting that this was the condition just before the entire encapsulation of the hematoma (Fig. 4 b). It used to be considered that a blood clot in the subdural space is needed to develop a chronic subdural hematoma. However, since the introduction of CT scan, there have been many reports suggesting that chronic subdural hematoma has developed from subdural fluid collection without apparent evidence of blood clot after head injury. Therefore, it has been controversial whether the blood clot is absolutely essential to develop into the chronic subdural hematoma or not.(ABSTRACT TRUNCATED AT 250 WORDS)     

Primary intracranial hypotension associated with chronic subdural hematoma--report of 2 cases

Low spinal fluid pressure syndrome is characterized by orthostatic headache aggravated in upright position. It is classified into two from etiological standpoint i.e. primary and secondary (most often seen after lumbar puncture). On the other hand, low spinal fluid pressure is one of the promoting factors of chronic subdural hematoma. We report 2 cases of primary low spinal fluid pressure syndrome (primary intracranial hypotension) associated with chronic subdural hematoma. Case 1 is a 47-year-old man who was admitted with disorientation following 2 week history of orthostatic headache. Spinal fluid pressure was 7mmH2O in the lateral recumbent position. CT scan revealed bilateral isodense chronic subdural hematoma. The subdural hematoma reaccumulated 17 days after the first operation. Case 2 is a 31-year-old woman who was admitted with 4 week history of progressive orthostatic headache accompanied by nausea and vomiting. Spinal fluid pressure was 0 mmH2O. CT scan and cerebral angiography showed bilateral chronic subdural hematoma. The hematoma reaccumulated 20 days after the first operation. Six cases including our two cases of primary intracranial hypotention associated with chronic subdural hematoma have been reported. When changes of characters of headache, especially mental symptoms and disturbances of consciousness occurred in patients with chronic orthostatic headache, association of chronic subdural hematoma should be suspected. In cases with chronic subdural hematoma associated with low spinal fluid pressure syndrome, the reaccumulation of hematoma tends to occur after burr hole opening and irrigation of hematoma.     

A case of septic aneurysm complicated with simultaneous subdural and intracerebral hematoma

A case of septic aneurysms complicated with simultaneous subdural and intracerebral hematoma is presented. A 13-year-old girl had been operated on for endocardial cushion defect when she was 5 years old, and residual mitral regurgitation was followed up. She suddenly complained of headache, vomited and lost consciousness. She was brought to the Tokyo Women's Medical College Hospital by an ambulance. On arrival, she was semicomatose. Her left pupil was mydriatic and did not react to light. Right hemiparesis was noted. Systolic murmur was audible in the apical region of the heart. Laboratory data showed a mild anemia and a white cell count of 23,000. CT scan showed a subdural hematoma in the left frontotemporoparietal region and a small subcortical hematoma in the left occipital lobe. An emergency operation was carried out for the subdural hematoma. When the dura was opened, about 10 ml bloody CSF flowed out. A hematoma weighing about 50 g was removed. A bleeding point or an aneurysm could not be discovered on the dura, arachnoid membrane or surface of the brain at the operation. On the 15th day after the operation, when the fever was decreased, cerebral angiography was done. The left vertebral angiogram showed an aneurysm on a peripheral branch of the calcarine artery, which was considered the origin of the subcortical hematoma in the left occipital lobe. The left carotid angiogram showed no aneurysm. On the seventh day after that study, the aneurysm did not appear by left vertebral angiography. She was discharged with no neurological deficit. One month later, she was admitted again with a high fever.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Chronic subdural hematoma following advanced cancer: report of three cases

Three cases of chronic subdural hematoma (CSH) following advanced cancer are reported. Case 1. A 54-year-old male patient was referred to our clinic in a semicomatose state. Bilateral CSH was evacuated through a pair of burr holes, and consciousness was recovered. However, subependymal hemorrhage occurred at the third ventricle 6 days after the operation. Hematological examination revealed thrombocytopenia. He died 12 days after operation because of hemorrhage in the lung. Postmortem examination disclosed metastatic adenocarcinoma of unknown origin to the dura mater, lymph nodes, lung and bone marrow. Case 2. A 50-year-old male patient who was diagnosed as having gastric cancer was referred to our clinic in a state of deep coma. CT scan revealed CSH and putaminal hemorrhage at the left side. Hematological examination revealed disseminated intravascular coagulation (DIC). After the subdural hematoma was evacuated, the putaminal hematoma enlarged and hemorrhagic infarction at the left temporo-occipital lobes occurred. He died 2 days after operation. Autopsy was not carried out, but histological examination revealed poorly differentiated malignant cells in the outer membrane of the subdural hematoma. Case 3. A 53-year-old female patient who had a history of gastric cancer operated on 4 years ago was admitted to our clinic complaining of headache and vomiting. CT scan revealed bilateral subdural hematoma. Following a pair of burr-holes and irrigation of the hematoma, hemorrhage recurred alternatively at the left side on the 6th and at the right side on the 27th day after the operation. Hematological examination revealed DIC, and bone marrow puncture disclosed metastasis of the adenocarcinoma.(ABSTRACT TRUNCATED AT 250 WORDS)     

Three-channeled aortic dissection; report of a case

The formation of 2 adjacent lumens is rarely observed in aortic dissection. We report herein a case of ruptured 3-channeled aortic dissection in a short time of hospitalization. A 58-year-old man who had been followed up for aortic dissection (Stanford type B) was admitted to Kumamoto National Hospital with an abdominal pain and a lumbago. A computed tomography (CT) revealed that a 3-channeled aortic dissection from the aortic arch to the right common iliac artery. An intramural hematoma was generated in the abdominal aorta and the left kidney was not enhanced. We initially adopted conservative therapies. But on the next day, he suddenly complained a severe back pain and died. At autopsy, the thoracic aorta was found to have ruptured into the mediastinum, and massive hematoma was formed.     

Acute brain edema in fatal head injury: analysis by dynamic CT scanning

Dynamic computerized tomography (CT) was performed on 42 patients with acute head injury to evaluate the hemodynamics and to elucidate the nature of fatal diffuse brain bulk enlargement. Patients were divided into two groups according to the outcome: Group A included 17 nonfatally injured patients, eight with acute epidural hematomas and nine with acute subdural hematomas; Group B included 25 fatally injured patients, 16 with acute subdural hematomas and nine with bilateral brain bulk enlargement. Remarkable brain bulk enlargement could be seen in all fatally injured patients with acute subdural hematoma. In 29 (69%) of 42 patients, dynamic CT was performed within 2 hours after the impact. In the nonfatally injured patients with brain bulk enlargement, dynamic CT scans suggested a hyperemic state. On the other hand, in 17 (68%) of the 25 fatally injured patients, dynamic CT scans revealed a severely ischemic state. In the fatally injured patients with acute subdural hematoma, CT Hounsfield numbers in the enlarged hemisphere (hematoma side) were significantly lower than those of the opposite side (p less than 0.001). Severe diffuse brain damage confirmed by follow-up CT scans and uncontrollable high intracranial pressure were noted in the fatally injured patients. Brain bulk enlargement following head injury originates from acute brain edema and an increase of cerebral blood volume. In cases of fatal head injury, acute brain edema is the more common cause of brain bulk enlargement and occurs more rapidly than is usually thought.