Suk-Hee Heo

Cerebral embolism of iodized oil (lipiodol) after transcatheter arterial chemoembolization for hepatocellular carcinoma.

Cerebral lipiodol embolism is a rare complication of transcatheter arterial chemoembolization (TACE). Its pathological mechanism remains ambiguous despite several investigations. In Case 1, a 67‐year‐old man with hepatocellular carcinoma (HCC) experienced neurological deficits soon after undergoing a fourth session of TACE. Computed tomography (CT) scan showed multiple hyperdense lesions along the gyrus of frontal lobes and in the subcortical white matter. Transcranial Doppler (TCD) and transesophageal echocardiogram performed during the intravenous injection of agitated saline documented the presence of a right‐to‐left shunt (RLS) by demonstrating microbubbles in the left middle cerebral artery and left atrium. In Case 2, a 63‐year‐old woman underwent a third TACE due to a large HCC. After the procedure, her mental status deteriorated. Brain CT showed multiple hyperdense lesions on the cerebral and cerebellar cortex. TCD with agitated saline showed multiple microembolic signals shortly after the injection of agitated saline. The risk of cerebral lipiodol embolism may increase with recurrence and progression of HCC in patients who have a pre‐existing RLS in the heart or lung. A test for the detection of an RLS may be necessary to identify patients with a heightened risk of cerebral embolism when multiple TACE procedures are required. TACE for HCC can cause pulmonary embolism or infarction. 1,2 However, cerebral lipiodol embolism is rare after TACE. There have been several reports of cerebral embolism after TACE, but their exact mechanism has not yet been fully elucidated. We report herein 2 patients who developed cerebral lipiodol embolism after undergoing multiple TACE procedures for remnant HCC through a pre‐existing RLS.

Transarterial embolization for postoperative hemorrhage after abdominal surgery

The study goal was to evaluate the efficacy, safety, and clinical outcome of transarterial embolization for postoperative hemorrhage after abdominal surgery. Thirty-three patients were referred for angiography because of gastrointestinal or intra-abdominal bleeding after abdominal surgery. Urgent angiography and transarterial embolization was performed in all 33 patients. The clinical and angiographic features were retrospectively reviewed. Angiography revealed a discrete bleeding focus in 26 (79%) of 33 patients. Transarterial embolization was technically successful in 24 (92%) of 26 patients with a discrete bleeding focus. Rebleeding occurred in four (17%) of 24 patients. They were successfully managed with repeat embolization. There was no procedure-related complication during follow-up period. Angiography has a high detection rate of bleeding site in patients with postoperative hemorrhage after abdominal surgery. Transarterial embolization is considered to be an effective and safe means in the management of postoperative hemorrhage.

Clinical outcomes of patients with acute minor stroke receiving rescue IA therapy following early neurological deterioration.

Background Patients presenting with minor ischemic stroke frequently have early neurological deterioration (END) and poor final outcome. The optimal management of patients with END has not been determined. Objective To investigate rescue IA therapy (IAT) when patients with acute minor ischemic stroke develop END. Methods This was a retrospective study of consecutively registered patients with acute minor stroke and END. ‘END’ was defined as an increase in National Institutes of Health Stroke Scale (NIHSS) scores by 1 or more points (or development of new neurological symptoms) and ‘ΔEND−NIHSS’ was defined as numerical difference between NIHSS scores at the time of END and before END. Rescue IAT following END was adjusted for the covariates to evaluate the association between IAT and favorable outcome at 3 months. Results Among 982 patients with acute minor ischemic stroke, END occurred in 232 (23.6%). Of the 209 patients with END with full data available, 87 (41.6%) had favorable outcomes at 3 months. Rescue IAT following END was performed in 28 (13.4%). Favorable 3-month outcomes were seen in 50% of patients undergoing rescue IAT, including 8/19 (42.1%) undergoing rescue IAT beyond 8 h. By multivariate logistic regression analysis, rescue IAT following END was independently associated with favorable outcome at 3 months (OR=10.9; 95% CI 3.06 to 38.84; p<0.001). Conclusions The results suggest that rescue IAT may be safe and effective when END occurs in selected patients with acute minor ischemic stroke. Further prospective and randomized studies are needed to confirm our results.

Aspirin Resistance in the Acute Stages of Acute Ischemic Stroke Is Associated with the Development of New Ischemic Lesions

Background Aspirin is a primary antiplatelet agent for the secondary prevention of ischemic stroke. However, if aspirin fails to inhibit platelet function, as is expected in acute ischemic stroke (AIS), it may increase the rate of early clinical events. Therefore, we sought to determine whether aspirin resistance in the acute stage was associated with early radiological events, including new ischemic lesions (NILs). Methods This study was a single-center, prospective, observational study conducted between April 2012 and May 2013. Aspirin 300 mg was initially administered followed by maintenance doses of 100 mg daily. The acute aspirin reaction unit (aARU) was consistently measured after 3 hours of aspirin loading. An aARU value ≥550 IU was defined as biological aspirin resistance (BAR). NILs on follow-up diffusion-weighted imaging (DWI) were defined as lesions separate from index lesions, which were not detected on the initial DWI. Results A total of 367 patients were analyzed in this study. BAR in aARU was detected in 60 patients (16.3%). On follow-up DWI, 81 patients (22.1%) had NILs, which were frequently in the same territory as the index lesions (79%), pial infarcts (61.7%), and located within the cortex (59.3%). BAR was independently associated with NILs on follow-up DWI (adjusted OR 2.00, 95% CIs 1.01–3.96; p = 0.047). Conclusion In conclusion, BAR in aARU could be associated with NILs on follow-up DWI in AIS. Therefore, a further prospective study with a longer follow-up period is necessary to evaluate the clinical implications of aARU in AIS.

Use of Antithrombotics after Hemorrhagic Transformation in Acute Ischemic Stroke

Backgrounds There have been neither appropriate guidelines nor clinical studies about the use of antithrombotics after hemorrhagic transformation (HT). We sought to find whether the use of antithrombotics after hemorrhagic infarction might be associated with aggravation of HT and neurological deterioration. Methods This retrospective study included prospectively registered consecutive patients with acute ischemic stroke and HT in our tertiary stroke center. We focused on the hemorrhagic infarction. Aggravation of HT was defined as either enlargement of the original HT or newly developed HT within the infarcted area by visual analysis. We analyzed relationships between antithrombotics and HT, and neurological deterioration after HT in patients with hemorrhagic infarction. In addition, we assessed composite outcomes including neurological deterioration, vascular events, and death at 1month after HT. We analyzed relationships between antithrombotics after discharge and composite outcomes within 1month after HT. Results 222 patients were finally analyzed. Of the 150 patients with hemorrhagic infarction, 75 (50.0%) were type 1. The use of warfarin after detection of hemorrhagic infarction more frequently increased aggravation of HT than did the use of antiplatelets (4 of 24 vs 3 of 69; p = 0.094), but neither warfarin nor antiplatelets caused more HT than no medication. In addition, the use of antithrombotics after hemorrhagic infarction was not significantly associated with neurological deterioration after HT. The frequency of composite events at 1months was significantly lower in patients treated with antithrombotics than those treated without (p = 0.041). Conclusion In conclusion, the results of this study suggest that antithrombotics can safely be used after hemorrhagic infarction and may not be associated with neurological deterioration and aggravation of HT. Further studies are needed to confirm our results.

Clinical Implications of Changes in Individual Platelet Reactivity to Aspirin Over Time in Acute Ischemic Stroke

Background and Purpose— Time-dependent changes in individual platelet reactivity have been detected in patients with coronary artery disease. Therefore, we sought to evaluate the time-dependent changes in platelet reactivity to aspirin during the acute stage after ischemic stroke and the clinical implications of variable patient responses to aspirin in acute ischemic stroke. Methods— We conducted a single-center, prospective, observational study. The acute aspirin reaction unit (ARU) was measured after 3 hours of aspirin loading, with higher values indicating increased platelet reactivity despite aspirin therapy. The follow-up ARU was measured on the fifth day of consecutive aspirin intake. The numeric difference between the follow-up ARU and the acute ARU was defined as &Dgr;ARU and was stratified into quartiles. Early neurological deterioration was regarded as an early clinical outcome. Results— Both the acute ARU (476±69 IU) and the follow-up ARU (451±68 IU) were measured in 349 patients in this study. Early neurological deterioration was observed in 72 patients (20.6%). Changes in aspirin platelet reactivity over time showed an approximately Gaussian distribution. The highest &Dgr;ARU quartile was independently associated with early neurological deterioration (odds ratio, 3.19; 95% confidence interval, 1.43–7.10; P=0.005) by multivariate logistic regression analysis. Conclusions— The results of our study showed that the increase in platelet reactivity to aspirin over time is independently associated with early neurological deterioration in patients with acute ischemic stroke. In addition, during the acute stage of ischemic stroke, serial platelet reactivity assays may be more useful than a single assay for identifying the clinical implications of aspirin platelet reactivity after ischemic stroke.

Cerebral Actinomycosis : Unusual Clinical and Radiological Findings of an Abscess

We report a case of cerebral actinomycosis in a 69-year-old immunocompetent woman. The patient showed a progressive worsened mental status for one week. MRI examination showed an increased size of multiple enhancing nodular lesions associated with mild perilesional edema. We performed an open biopsy for the right frontal enhancing lesion. The intraoperative finding showed a yellowish friable lesion that was not demarcated with normal tissue. Pathologically, an actinomycotic lesion with sulfur granules and inflammatory cells was diagnosed. We report an unusual case of diffuse involvement of cerebral actinomycosis. The presence of the uncapsulated friable lesion that consisted mainly of foamy macrophages and lymphocytes could explain the unusual radiological features.

Lobar cerebral microbleeds associated with transient focal neurological symptoms followed by symptomatic intracerebral hemorrhage.

Cerebral microbleeds (CMBs) are defined as all discrete round-shaped hypointense areas on T2*-weighted magnetic resonance images (MRIs) with a gradient-echo (GRE) sequence [11]. CMBs can be regarded as a marker of vessel wall disorders with a higher tendency for intracerebral hemorrhage (ICH) [11]. It has been suggested that microbleeds increase the risk of ICH following antithrombotic administration for acute ischemic stroke [9, 14], though this issue remains controversial. In addition, there have been few reports of symptomatic ICH that has occurred at the site of microbleeds in the literature [2, 13]. However, these lesions themselves have been considered asymptomatic. We present a case of CMBs presenting with transient neurologic symptoms that developed into subsequent ICH. A 65-year-old man with no previous neurological history visited our hospital because of incoherent speech and headache. He had a history of diabetes mellitus and chronic hepatitis B. He had been diagnosed with hepatocellular carcinoma prior to this presentation. Neurological examination revealed that he had language disturbances with jargon speech and abnormal comprehension. These symptoms fluctuated and persisted for about half an hour after symptom onset. The results of other physical examinations were normal. Electroencephalography showed that there were no epileptiform discharges or abnormal inherent rhythms. There were also no acute ischemic brain lesions or hemorrhages on initial brain MRI (Fig. 1a). GRE images showed multiple CMBs in the left temporo-parieto-occipital lobe relevant to language disturbance (Fig. 1b). However, there were no CMBs in the deep subcortical area and brainstem. There were no CMBs on previous GRE images obtained at a local clinic 1 month prior to this presentation as well (Supplemental Figure). While he had no symptoms at this time, he underwent brain MRI as part of a medical check-up. All laboratory tests, including coagulation profiles, were normal. He was tentatively diagnosed with (1) recurrent transient ischemic attacks and (2) mood disorder associated with medical condition. During admission, he was treated with antihypertensive agents and 100 mg of aspirin for prevention of secondary ischemic stroke. On the fourth day of admission, he suddenly developed global aphasia and right hemiparesis. Follow-up GRE images showed a large lobar hematoma with perilesional edema in the left temporo-parietal lobe where the CMBs were previously seen (Fig. 1c). Although he was referred to the Department of Neurosurgery for surgical management, he was discharged with a modified Rankin scale of 5. Our case illustrates that localized CMBs can be related to transient neurological symptoms and subsequent ICH. Although this is a single case that represents a causal relationship between CMBs and transient neurological symptoms, the association between CMBs and subsequent ICH could not be clarified, suggesting that transient Electronic supplementary material The online version of this article (doi:10.1007/s00415-012-6504-8) contains supplementary material, which is available to authorized users.

Gross Hematuria Associated with Genitourinary Tuberculosis

A 27-year-old man presented to the emergency department with sudden onset of massive gross hematuria and urinary retention. Contrast-enhanced computed tomography imaging showed uneven, dilated calices and a narrowing of the renal pelvis in the left kidney; in addition, a large hematoma was noted in the urinary bladder. An emergency cystoscopy was performed following detection of the hematoma and blood clots were removed. A lesional biopsy, a tuberculosis (TB) culture, and urine cytology showed positive results for Mycobacterium tuberculosis. The clinical manifestations of genitourinary tuberculosis are nonspecific and are usually detected at a chronic stage. In conclusion, we report an unusual cause of acute kidney injury associated with a subacute stage of genitourinary tuberculosis that caused mucosal erosion and bleeding in the bladder.