Haris Kamal

Posterior reversible encephalopathy syndrome secondary to blood transfusion

The appearance of posterior reversible encephalopathy syndrome (PRES) after blood transfusion is rare and has only been reported in three patients to our knowledge. We report a fourth patient with PRES secondary to blood transfusion. A 36-year-old woman with a history of menorrhagia presented to the emergency department with severe fatigue. She had a hemoglobin of 1.7 g/dl and received four units of red blood cells over 15 hours. On day 6 post-transfusion she returned with confusion, headache and a generalized tonic-clonic seizure. The MRI of her brain was consistent with PRES. The following day her confusion worsened, repeat MRI of the brain showed new T2-weighted lesions. Over next 10 days her mental status gradually improved close to her baseline. A repeat MRI of the brain showed resolution of the T2-weighted lesions. The clinical presentation, radiological findings and disease progression in our patient was consistent with PRES. Other than the blood transfusions, there were no apparent risk factors for PRES. The prior three patients with post-transfusion PRES have been reported in middle-aged women with uterine fibroids. It is suspected that these patients have a subacute to chronic anemic state due to ongoing menorrhagia. It is interesting to note that no cases of PRES post-transfusion have been reported in the setting of acute blood loss, such as from trauma. It is postulated that an abrupt increase in hemoglobin causes a rapid rise in blood viscosity and loss of hypoxic vasodilation. Subsequent endothelial damage and brain capillary leakage results in PRES. This constellation of changes may not occur after transfusion in patients with more acute blood loss.

Is acute reperfusion therapy safe in acute ischemic stroke patients who harbor unruptured intracranial aneurysm

Background Intracranial aneurysms are currently considered as contraindication for intravenous thrombolysis in acute ischemic stroke, very likely due to a possible increase in the risk of bleeding from aneurysm rupture; however, there is limited data available on whether intravenous thrombolysis is safe for acute ischemic stroke patients with pre-existing intracranial aneurysms. Aims and/or hypothesis To find out the safety of intravenous thrombolysis in acute ischemic stroke patients who harbor unruptured intracranial aneurysms. Methods We retrospectively reviewed the medical records and cerebrovascular images of all the patients treated with intravenous thrombolysis for acute ischemic stroke in our center from the beginning of 2006 till the end of April 2014. Those with unruptured intracranial aneurysm present on cerebrovascular images prior to acute reperfusion therapy were identified. Post-thrombolysis brain imaging was reviewed to evaluate for any intraparenchymal or subarachnoid hemorrhage related or unrelated to the aneurysm. Results A total of 637 patients received intravenous thrombolysis for acute ischemic stroke in our center during an 8.3-year period. Thirty-three (5.2%) were found to have at least one intracranial aneurysms. Twenty-three (70%) of those received only intravenous thrombolysis, and 10 patients received combination of intravenous and intra-arterial throm-bolysis. The size of the largest aneurysm was 10 mm in maximum diameter (range: 2-10 mm). The mean size of aneurysms was 4.8 mm. No symptomatic intracranial hemorrhage occurred among the 23 patients receiving only intravenous thrombolysis. Out of those who received a combination of intravenous and intra-arterial thrombolysis, one developed symptomatic intracranial hemorrhage in the location of acute infarct, distant to the aneurysm location. Conclusion Our findings suggest that neither intravenous thrombolysis nor combination of intravenous and intra-arterial thrombolysis increases the risk of aneurysmal hemorrhage in acute ischemic stroke patients who harbor unruptured intracranial aneurysms less than 10 mm in diameter. Their listing in exclusion criteria for intravenous throm-bolysis should be reconsidered to assure appropriate use of acute reperfusion therapy in this group of patients.

Whole brain CT perfusion deficits using 320-detector-row CT scanner in TIA patients are associated with ABCD2 score

Background: Transient ischemic attacks (TIA) are cerebral ischemic events without infarction. The uses of CT perfusion (CTP) techniques such as cerebral blood volume (CBV), time to peak (TTP), mean transit time (MTT) and cerebral blood flow (CBF) provide real time data about ischemia. It has been shown that CTP changes occur in less sensitive CTP scanners in patients with TIA. Larger detector row CTP (whole brain perfusion studies) may show that CTP abnormalities are more prevalent than previously noted. It is also unclear if these changes are associated with TIA severity. Objective: To demonstrate that TIA patients are associated with perfusion deficits using whole brain 320-detector-row CT perfusion, and to determine an association between ABCD2 score and perfusion deficit using whole brain perfusion. Methods: We retrospectively reviewed all TIA patients for CTP deficits from 2008–2010. Perfusion imaging was reviewed at admission; and it was determined if a perfusion deficit was present along with vascular territory involved. Results: Of 364 TIA patients, 62 patients had CTP deficits. The largest group of patients had MCA territory involved with 48 of 62 patients (77.42%). The most common perfusion abnormality was increased TTP with 46 patients (74.19%). The ABCD2 score was reviewed in association with perfusion deficit. Increased age >60, severe hypertension (>180/100 mmHg), patients with speech abnormalities, and duration of symptoms >10 min were associated with a perfusion deficit but history of diabetes or minimal/moderate hypertension (140/90–179/99 mmHg) was not. There was no association between motor deficit and perfusion abnormality. Conclusion: Perfusion deficits are found in TIA patients using whole brain CTP and associated with components of the ABCD2 score.

Effect of heparin on recanalization in acute stroke patients with intra-arterial thrombi

Anticoagulant use, such as heparin, is usually contraindicated in acute stroke patients. We present a study of patients, who were treated with intravenous heparin after a stroke that were also found to have an intraluminal thrombus. Prior studies imply that recanalization is achieved with heparin; however heparin should only prevent thrombus propagation. Therefore it is unclear whether and how IV heparin can achieve recanalization of intraluminal thrombi in acute stroke patients. A retrospective review of all acute stroke patients from a single stroke center who received a therapeutic IV heparin infusion from 5/2006 to 9/2011 were included in the study. We compared patients who had complete/partial recanalization and/or improved flow versus those that did not, with both these groups on a standard intravenous heparin infusion protocol. Demographic data was compared between the groups. Average partial thromboplastin time (PTT) during heparin infusion, time between computed tomography angiographies (CTAs), time from stroke onset to receiving IV heparin, and vessel occluded were also compared between groups. Forty-one patients (19 female, 22 male) were included in the study with a total of 55 vessels (either carotid, middle cerebral artery, anterior cerebral artery, posterior cerebral artery/posterior circulation) having intraluminal thrombi; 31 patients had 41 vessels with either partial or complete recanalization of effected vessels, while 10 patients had 14 vessels that did not have at least one vessel recanalize while on heparin. Using t-test we noted that the average PTT between the vessels that had partial/complete recanalization group (61.74) and nonrecanalization group (66.30) was not statistical significantly different (P=0.37).The average time in days on heparin between vascular imaging studies (CTA/conventional angiogram) in the group of vessels with partial/complete recanalization (7.12 days) and the ones with no change (6.11 days) was not significantly different between the two groups (P=0.59). Patient’s vessels receiving heparin for <24 hours versus those >24 hours did not significantly differ either (P=0.17). This study compares patient characteristics associated with recanalization of intraluminal thrombi in acute stroke patients on heparin. Recanalization of intraluminal thrombi are not associated with average PTT or duration on heparin.

Safety of intravenous thrombolysis for acute ischemic stroke in patients with preexisting intracranial neoplasms: a case series

Intracranial neoplasms are currently considered a contraindication for intravenous (IV) thrombolysis in acute ischemic stroke (AIS) patients (1,2). Minimal data are available on the safety of IV thrombolysis for AIS in patients with preexisting intracranial neoplasm. We sought to determine the safety of IV recombitant tissue plasminogen activator (rtPA) in such patients through a retrospective hospital-based study. We retrospectively reviewed the medical records of patients who received IV rtPA for AIS from January 2006 to April 2014 at our tertiary academic medical center. All patients were treated based on the standard protocol adopted from the American Heart Association/ American Stroke Association within 4.5 h of AIS onset (2). Patients who received intra-arterial (IA) thrombolysis after IV rtPA were included. A subset of patients with definite intracranial neoplasms from this cohort was identified. Follow-up computed tomography (CT) or magnetic resonance imaging (MRI) within 24 to 36 h of IV rtPA administration and medical records were reviewed to determine the number of patients with symptomatic intracranial hemorrhage (sICH) in this subset. sICH was defined as intracranial hemorrhage (ICH) with an increase in National Institutes of Health Stroke Scale of at least 4 points (3). In addition, hemorrhage within the neoplasm was evaluated. Six hundred thirty-seven patients received full dose IV rtPA for AIS within the study period. Preexisting intracranial neoplasms were found in 13 of the 637 patients reviewed (2%). The demographics of the patients are outlined in Table 1. None of the 13 patients developed sICH or hemorrhage into the tumor after thrombolysis. To the best of our knowledge, our study is the largest on the safety of IV rtPA for AIS in patients with preexisting intracranial neoplasms. This study is also the first report, to our knowledge, of patients with intracranial neoplasm who received IV rtPA followed by IA thrombolysis with mechanical thrombectomy devices. Our study should be interpreted in light of several limitations. It is a single-center study with a low number of cases; in addition, we have no malignant neoplasm in our cohort and no generally valid conclusion can be drawn about the safety of IV thrombolysis in all grades of intracranial neoplasm. Our finding suggests that IV rtPA administration for AIS does not increase the risk of hemorrhage within the neoplasm in patients with preexisting benign intracranial neoplasm. Their listing in exclusion criteria for rtPA should be reconsidered to assure appropriate use of IV rtPA in this group of patients. We hope our study will encourage other centers to look into their data and study this further, so as to determine the actual risk of hemorrhage with rtPA in patients with intracranial neoplasms.

Intravenous Thrombolysis for Acute Ischemic Stroke in Patients with Thrombocytopenia

OBJECTIVE To determine the safety of intravenous (IV) recombinant tissue plasminogen activator (rtPA) in patients with acute ischemic stroke (AIS) who had a platelet count <100,000 /mm3. METHODS We reviewed the charts of all patients who received IV rtPA for AIS during a 9.6-year period at our stroke center. Those with platelets <100,000/mm3 were identified. Head computed tomography scans performed in 24-36 hours postthrombolysis were reviewed to evaluate the rate of symptomatic intracranial hemorrhage (sICH). RESULTS A total of 835 patients received IV rtPA for AIS during this period. A total of 5 patients were identified to have a platelet count <100,000/mm3. One of them (20%) developed sICH post-IV tPA administration .The mean platelet count of those 5 patients was 63,000 ± 19,000/mm3. To the best of our knowledge, only 21 thrombocytopenic patients have been reported to receive IV rtPA for AIS in the medical literature. Combining our 5 cases with 21 patients previously reported, we have 26 AIS patients who had a platelet count <100,000/mm3 and received IV rtPA, with 2 of them developing sICH (7.7 %). Comparing the rate of sICH among this group with the patients with normal platelet count in our cohort, there was no statistically significant difference (7.7% versus 6.04%, P value = .73). CONCLUSION IV rtPA for AIS might be safe in patients with platelet count <100,000/mm3 and it is reasonable not to delay IV rtPA administration while waiting for the platelet count result, unless there is strong suspicion for abnormal platelet count.

Intravenous and Arterial Treatments for Acute Ischemic Stroke: Indications and the Role of Imaging.

Abstract Acute ischemic stroke continues to be a leading cause of disability in adults and the fifth leading cause of mortality worldwide. In the past few years, acute ischemic stroke diagnosis and management has advanced by leaps and bounds, with the lengthening of the time window for intravenous tissue plasminogen activator and the establishment of endovascular stroke therapy. As a result of these changes, the focus today has shifted from proving efficacy to expanding indications and identifying all patients who may benefit from these therapies. In this pursuit, neuroimaging will continue to play a pivotal role, by shifting treatment paradigms from time-based to tissue-based. The quest to accurately determine the volume and function of salvageable brain has never been more important than now.

Omega-3 fatty acid ethyl esters do not improve clopidogrel associated P2Y12 inhibition in stroke patients

The specific action of omega-3 fatty acid ethyl esters (OFA) in preventing cerebrovascular disease remains unknown, but research has demonstrated multiple possible mechanisms. In addition to altering lipid profiles, OFA may inhibit platelet aggregation. Clopidogrel inhibits platelets via the P2Y12 receptor. OFA may alter clopidogrel-associated platelet-inhibition via a possible combined effect on P2Y12 inhibition. To determine if OFA affects clopidogrel associated P2Y12 platelet receptor inhibition by comparing the percentage of responders in patients with cerebrovascular disease who were taking clopidogrel with or without OFA. We retrospectively reviewed data from adult patients with cerebrovascular disease or cerebral aneurysms and taking clopidogrel, who were seen at a single hospital between March 2010 to September 2011. We included 438 subjects in the study. For the 67 subjects who received loading doses of both clopidogrel and OFA, 71.6% had a P2Y12 inhibition response more than 20%, which is considered a positive response. For the 55 subjects who received just clopidogrel load, 67.2% of subjects were responders. There were 70.4% responders in the 274 subjects who were taking 75 mg of clopidogrel alone at home, and 73.8% responders in the 42 subjects who were taking both clopidogrel and OFA at home. However, these percentage differences were not statistically significant. This study did not find additional P2Y12 platelet inhibition when patients were given OFA, either given as a loading dose or taking it daily.

Appendicular ataxia without position sense loss in a patient with parietal lobe infarct

A 86-year-old lady presented with sudden onset of appendicular ataxia of the right arm with minimal weakness and no deep sensory loss. On neurological exam, she hadminimal pronator drift. She had undershooting and overshooting on attempting to reach the target finger on finger to nose test. She also has dysdiadokokinesia and uncontrolled rebound. The tests were not worsened with eyes closed. The sensory exam was unremarkable including normal proprioception. Her brain MRI showed an area of acute infarct in left posterior parietal lobe (Fig. 1) and no other lesion. Although parietal ataxia is generally considered to result from loss of proprioceptive feedback inputs to the motor function [1], but our patient showed clinical features of classic cerebellar kinetic ataxia without loss of proprioception. Brain MRI showed

Prior Asymptomatic Parenchymal Hemorrhage Does Not Increase the Risk for Intracranial Hemorrhage after Intravenous Thrombolysis.

Background: The NINDS trial demonstrated the efficacy of intravenous (IV) recombinant tissue plasminogen activator (rtPA) in improving the neurologic outcome in patients presenting with acute ischemic strokes. Patients who had a prior history of intracranial hemorrhage (ICH) were excluded from this trial, possibly due to a hypothetical increase in the subsequent bleeding risk. Thus, there is little data available, whether against or in favor of, the use of IV rtPA in patients with prior ICH. We aim to aid in determining the safety of IV rtPA in such patients through a retrospective hospital-based single center study. Methods: We reviewed the brain imaging of all patients who received IV rtPA at our comprehensive stroke center from January 2006 to April 2014 for evidence of prior ICH at the time of IV rtPA administration. Their outcomes were determined in terms of subsequent development of symptomatic ICH as defined by the NINDS trial. Results: Brain imaging for 640 patients was reviewed. A total of 27 patients showed evidence of prior ICH at the time of IV thrombolysis, all intra-parenchymal. Only 1 patient (3.7%) developed subsequent symptomatic ICH after the administration of IV rtPA. Of the remaining 613 patients who received IV rtPA, 25 patients (4.1%) developed symptomatic ICH. Conclusion: This retrospective study provides Level C evidence that patients with imaging evidence of prior asymptomatic intra-parenchymal hemorrhage presenting with an acute ischemic stroke do not show an increased risk of developing symptomatic ICH after IV thrombolysis.