Intracranial hemorrhage is a common, potentially lethal complication of anticoagulant therapy including warfarization. Anticoagulant-related intracranial hemorrhage propounds a difficult clinical selection: maintaining anticoagulant therapy may extend the volume of the hematoma, early resumption of anticoagulation therapy may cause recurrence of hemorrhage, and correction of the coagulopathy may put patients at risk for thromboembolism involving the brain. Particularly, the risk of thromboembolic events may also be greater for patients with mechanical valves prosthesis in the mitral portion with atrial fibrillation. This dilemma on treatment of the patients exists because of a lack of data for a large series. We examined the medical records and CT scan findings for a consecutive group of patients admitted with non-traumatic anticoagulant-related intracerebral hematoma. We reviewed neurological presenting data, cardiac risk factors for systemic thromboembolism, and hospital management. We analyzed the management of warfarin-related intracerebral hemorrhages in 32 patients with cardiac disease, evaluating the degree of anticoagulation via the thrombotest. Anticoagulants were discontinued immediately after diagnosis of intracerebral hematoma was established by CT scan. Patients with mechanical valve prosthesis patients, who required intensive long-term anticoagulant therapy, constituted the majority of our series (53.1%). Five patients had experienced previous transient ischemic attacks or minor strokes, and 19 had hypertension. The type of intracerebral hematoma was subcortical hematoma (n=13), thalamic hemorrhage (n=11), putaminal hemorrhage (n=4), pontine hemorrhage (n=3), or cerebellar hemorrhage (n=1). Vitamin K was administered in all patients and 3 who demonstrated low thrombotest values received FFP intraoperatively. Seven patients underwent evacuation of hematoma, and in 4 patients with thalamic hemorrhage accompanied by ventricular rupture ventricular drainage was carried out. Intraoperative hemostasis was brought under control at the time of surgery. However, in 1 patient, thalamic hematoma enlarged postoperatively with a fatal outcome within 6 days of surgery even without resumption of anticoagulant therapy. Early resumption of anticoagulant therapy (within 3 days) did not cause intracerebral rebleeding in any operative patients. Only 1 patient developed vertebrobasilar system infarction and died despite early resumption of anticoagulant therapy. Some of the subcortical hematoma patients had a good outcome. Temporary interruption of anticoagulant therapy within 3 days seems safe for patients with intracerebral hematoma. Aggressive surgical intervention should particularly be performed in patients with anticoagulant-related subcortical hematoma, as in the case of anticoagulant-unrelated parenchymal hematoma.
We retrospectively analyzed 40 cerebral apoplectic patients with renal failure. Diagnoses included intracerebral hemorrhage (ICH) in 26, subarachnoid hemorrhage (SAH) in 12, intraventricular hemorrhage in 1 and hemorrhagic infarction in 1. Treatment for renal failure was continuous ambulatory peritoneal dialysis (CAPD) in 24, hemodialysis (HD) in 8 and continuous hemodiafiltration (CHDF) in 8. Conservative treatment was performed in 21 of 26 ICH patients. Surgical repair with neck clipping was performed in 8 of 12 SAH patients. Endovascular treatment with Guglielmi detachable coil was performed in 1. The mortality rate with ICH and SAH was 31% and 67%, respectively. The major risk factors were hemorrhagic tendency and initial damage to the brain. The hemorrhagic tendency in CAPD, HD and CHDF was 8%, 25% and 25%, respectively. Brain edema was not a major problem in each of the 3 methods. Extracorporeal circulation using anticoagulant agents in HD and CHDF was also considered to account for the high incidence of hemorrhagic tendency. As compared with HD and CHDF, CAPD was considered more appropriate for the cerebral apoplectic patients with renal failure. Early initiation and frequent dialysis with CAPD are crucial to the effective treatment for such patients.
Patients with carotid artery stenosis frequently have other systemic disease such as hypertension, diabetes mellitus and ischemic heart disease. For better prognosis after carotid endarterectomy (CEA) management of these systemic diseases is essential. On the other hand, systemic management for cerebral ischemia during cross-clamping of the internal carotid artery (ICA) at CEA and postoperative hyperperfusion after CEA are also needed. The purpose of this study is to develop a rational plan for the systemic management of patients undergoing CEA. In 154 patients with carotid artery stenosis 168 CEAs were done. T-shaped intraluminal shunt was used in all patients. The average age of the patients was 63 years. The average degree of stenosis on the operated side was 66%. Fifty-seven of the patients had hypertension, 32% had hyperlipidemia, 22% had ischemic heart disease, and 20% had diabetes mellitus. Coronary angiography was done in 16 patients, and significant coronary artery stenosis was seen in 12 patients. Coronary arteries were reconstructed in 7 of these patients. Coronary artery bypass grafting (CABG) was done in 1 patient and PTCA in 1 patient before CEA. In 6 patients the coronary artery was reconstructed after CEA. Simultaneous CEA and CABG were not performed. There was no cardiac complication during CEA. The management strategy for simultaneous carotid artery stenosis and coronary artery disease depends on the hemodynamic severity of each disease. In patients with poor collateral circulation, cross-clamping of the ICA will induce cerebral ischemia. Somatosensory evoked potential (SEP) was more sensitive for detection of cerebral ischemia during ICA cross-clamping than other monitorings of ICA stump pressure and cerebral oxyhemoglobin concentration. The shunt system was useful for decreasing time of ischemia. Hyperperfusion could be predicted by marked increase (≥180ml/min) in ICA flow after CEA and by increased flow velocity of the middle cerebral artery (MCA), which could be measured by transcranial Doppler sonography. As MCA flow velocity after CEA increases until 2 days after CEA, systemic arterial blood pressure must be controlled until several days after CEA. When control of blood pressure is difficult, barbiturate treatment should be considered.
Hypothermic anesthesia (HTA) in aneurysmal surgery is a useful and effective tool for preventing possible ischemic or mechanical damage to the brain caused by surgical manipulations. From the viewpoint of clinical use, HTA can be divided into three groups: mild HTA (35-33°C), moderate HTA (33-27°C) and deep HTA (20°C-). We have been using moderate HTA in surgery for formidable aneurysms since 1980. The recent anesthesiological advances in this field enabled us to use mild HTA for a wider range of cases with subarachnoid hemorrhage and deep HTA for restricted cases. During the last 7 years, 282 aneurysmal surgeries were carried out and 166 (58.9%) were under HTA. The use of HTA significantly increased in the last 3 ('96-'98) of these 7 years: 66.4% vs. 54%, P<0.05. From the review of our own experiences in HTA, we recommend the expanded utilization of HTA for aneurysmal surgery with satisfactory safety. To minimize damage to the brain tissue in cases with considerable surgical insults expected, mild HTA is a tool of choice. The use of HTA is also indicated for operations for multiple or bilaterally located aneurysms or for cases with tight brain caused by the existence of intracerebral hematoma or brain edema at the acute stage. Furthermore, mild HTA may well be used in every early surgery because of its clinical safety and ease of use. Moderate HTA, requiring more complicated techniques and assistance of experienced anesthesiologists, brings further increased tolerance to ischemic insults to the brain. Cases with supratentorial large or giant aneurysm or with internal carotid aneurysm, which are difficult to clip for a long without time without causing parent artery occlusion are good candidates for moderate HTA as well as those with basilar trunk aneurysm. Techniques of PCPS allow us to use deep HTA, which is less invasive than the open-chest method, and we can adopt this tool for extremely difficult operations like clipping of deeply seated giant or complicated and posing aneurysm such as the two cases presented in this report.
We retrospectively analyzed the postoperative management of elderly patients with ruptured cerebral aneurysms and designed management policies for such cases. Sixty consecutive patients over the age of 70 years with ruptured cerebral aneurysms were operated on in an acute stage at our institution until 1998. The patients were classified as preoperative clinical grade and surgical outcome into four groups: 19 patients were Grade I to II according to the clinical grading scale of Hunt and Kosnik and recovered skills of daily living (Group 1), 8 patients were Grade I to II and had unfavorable outcomes (Group 2), 6 patients were Grade III to IV and had favorable outcomes (Group 3), and 27 patients were Grade III to IV and had unfavorable outcomes (Group 4). In Group 1 and 3, the level of consciousness became alert and all cases were able to eat within a few days after the clipping of aneurysms. Mild hypoalbuminemia and hyponatremia were found in many of the cases. Although general complications required some treatment in over 70% of the cases, they resulted in the favorable outcomes. In a few cases in Group 2 and 4, the level of consciousness improved after the operation but the patients were unable to eat. Marked hypoalbuminemia and sodium imbalance caused symptomatic vasospasm and general complications, which were responsible for the unfavorable outcomes. In elderly patients with ruptured cerebral aneurysms, the recovery of consciousness as early as possible after the operations is required to achieve favorable outcome. Under sustained postoperative disturbance of consciousness, extensive care should be taken in the management of fluid and electrolyte balance, and nutrition.
The prognosis of residual neck following clipping surgery is not sufficiently documented. The purpose of this study is to determine the serial changes of residual neck after clipping surgery. Between 1974 and 1997, 22 patients under the age of 70 years with residual neck were followed by serial angiographies for a mean of 3.4 years (range 1 year to 9 years). Initial angiography was performed 1 year after the surgery and further studies were done every 1-2 years subsequently. The location of aneurysms were 13 internal carotid artery (IC)(1 IC-cave, 1 IC-ophthalmic, 7 IC-posterior communicating artery, 2 IC-anterior choroidal artery, 2 carotid-bifurcation), 7 middle cerebral artery, 1 anterior communicating artery and 1 peripheral anterior cerebral artery. The results showed 18 residual necks remained unchanged, 3 were obliterated spontaneously after 1 year, 1 year and 3 years respectively from the surgery, and 1 was enlarged after 6 years. Two important issues were clarified. First, residual necks should be observed with serial angiographies since the regrowth from residual neck is possible. Second, in the initial clipping surgery, we must seek to achieve complete clipping without residual neck using special techniques such as intraoperative endoscope.
The presence of significant multifocal vascular disease indicates an advanced stage of atherosclerosis. The coexistence of significant obstructive cerebrovascular disease or cervical carotid stenosis and coronary artery disease presents a difficult combination for surgical intervention. With the aim of reducing the risk of perioperative cardiovascular events, we did a comparative analysis of preoperative cardiovascular conditions and surgical results. According to ACC/AHA Task Report (Guidelines for Perioperative Cardiovascular Evaluation for Noncardiac Surgery), it is important to evaluate surgery-specific risk, clinical predictors of increased perioperative cardiovascular risk, and functional capacity. When there are major predictors of clinical risk, cancellation or delay of surgery is advisable until the risk has been reduced. Patients with intermediate predictors of clinical risk and poor functional capacity have a likelihood of perioperative cardiac events as demonstrated with 2 of our cases. Patients with intermediate or minor predictors of clinical risk and moderate or excellent functional capacity can generally undergo surgery with little perioperative cardiac risk. Patients will require a careful consideration of clinical, surgery-specific, and functional status before a decision can be made as to whether to proceed to surgical intervention.
There seems to be a general agreement that unruptured cerebral aneurysms measuring more than 10mm should be treated surgically, although the situation regarding smaller lesions, especially those with a maximum diameter less than 5mm, is more controversial. We analyzed operative findings of 122 unruptured cerebral aneurysms found in 92 surgical cases to estimate whether such small aneurysms are prone to rupture. Among the 122, 32 (26%) were evaluated as having thick-walled sacs (type 1), 54 (44%) partially or entirely thin-walled sacs (type 2), and 36 (30%) partially or entirely very thin-wall sacs so that intra-aneurysmal blood turbulence was visible through the aneurysmal walls (type 3). The sizes were 9.6±1.3mm (mean±1 SD) for type 1 aneurysms, 4.8±0.3mm for type 2, and 5.3±0.9 mm for type 3, types 2 and 3 aneurysms being significantly smaller than type 1 aneurysms. Eighty-three percent of unruptured aneurysms less than 5 mm in diameter had partially or entirely thin-walled sacs. Ninety-eight percent of patients with surgical treatment for unruptured aneurysms less than 5 mm showed good recovery. Assuming that thin-walled aneurysms are at a high risk of subsequent subarachnoid hemorrhage, prophylactic surgical treatment for small unruptured aneurysms in otherwise healthy individuals may be recommended.
Systemic inflammatory response syndrome (SIRS) is the clinical expression of the action of complex intrinsic mediators of the acute phase reaction, and is a warning sign of multiple organ dysfunction syndrome (MODS) and poor outcome in various insults. Subarachnoid hemorrhage (SAH) also causes an inflammatory reaction and may lead to ischemic damage. We studied the predictive value of the SIRS for the occurrence of symptomatic vasospasms in 101 patients with aneurysmal subarachnoid hemorrhage. The patients were classified into three groups, according to the continuance of SIRS as follows: Group A (the presence of SIRS on admission/the presence of SIRS at the postoperative first day: SIRS+/+), Group B (SIRS+1 or SIRS -/+) and Group C (SIRS-/-). The correlation between the status of SIRS and the development of delayed ischemic neurological deficits was analyzed. Twenty-nine (28.7%) patients met the criteria for SIRS on admission. Postoperatively, 22 (21.8%) patients developed SIRS. Ten (10.0%) patients were assigned to Group A, 31 (30.7%) to Group B, and 60 (59.3%) to Group C. Thirty-five (33.6%) of the patients developed DIND. The incidence of DINDs was 90% (9/10) in Group A, and 35.5% (11 of 31) in Group B, and 25.0% (15 of 60) in Group C. There was a significant difference between the three groups. In addition, the outcome was significantly related to the presence of SIRS. The present study shows that sustained SIRS has a predictive value regarding the occurrence of symptomatic vasospasm following aneurysmal surgery.
A-37-year-old man suffered sudden severe occipital pain with vertigo, vomiting, diplopia, tetraparesis and hypalgesia of extremities, which continued for about half an hour. On admission, he complained of moderate occipital pain without neurological deficit. No abnormality was shown on CT scan, and CSF by spinal tap was clear. Dissecting aneurysms of both vertebral arteries was suspected on MRA and MRI. Typical pearl-and-string sign of both vertebral arteries was demonstrated on vertebral angiogram. So, conservative therapy with careful observation of serial MRA and angiogram was planned. Progression of dissection at one month later and the regression of dissection on four months later were demonstrated, although he has had no symptoms during this course. Ischemic-type dissecting aneurysms tend to cure at the chronic stage, while these findings show various changes on angiogram at the acute stage. If there is no worsening of the clinical symptoms, conservative therapy is the treatment of choice in spite of the progression of the dissection for the ischemic-type dissecting aneurysm.