James Guth

Desmopressin Improves Platelet Activity in Acute Intracerebral Hemorrhage

Background and Purpose— Minimizing hematoma growth in high-risk patients is an attractive strategy to improve outcomes after intracerebral hemorrhage. We tested the hypothesis that desmopressin (DDAVP), which improves hemostasis through the release of von Willebrand factor, improves platelet activity after intracerebral hemorrhage. Methods— Patients with reduced platelet activity on point-of-care testing alone (5), known aspirin use alone (1), or both (8) received desmopressin 0.4 &mgr;g/kg IV. We measured Platelet Function Analyzer-epinephrine (Siemens AG, Germany) and von Willebrand factor antigen from baseline to 1 hour after infusion start and hematoma volume from the diagnostic to a follow-up computed tomographic scan. Results— We enrolled 14 patients with of mean age 66.8±14.6 years, 11 (85%) of whom were white and 8 (57%) were men. Mean Platelet Function Analyzer-epinephrine results shortened from 192±18 seconds pretreatment to 124±15 seconds (P=0.01) 1 hour later, indicating improved plate activity. von Willebrand factor antigen increased from 242±96% to 289±103% activity (P=0.004), indicating the expected increase in von Willebrand factor. Of 7 (50%) patients who received desmopressin within 12 hours of intracerebral hemorrhage symptom onset, changes in hematoma volume were modest, −0.5 (−1.4 to 8.4) mL and only 2 had hematoma growth. One patient had low blood pressure and another had a new fever within 6 hours of desmopressin administration. Conclusions— Intravenous desmopressin was well tolerated and improved platelet activity after acute intracerebral hemorrhage. Larger studies are needed to determine its potential effects on reducing hematoma growth versus platelet transfusion or placebo. Clinical Trial Registration— URL: http://www.clinicaltrials.gov. Unique identifier: NCT00961532.

Surveillance neuroimaging and neurologic examinations affect care for intracerebral hemorrhage

Objective: We tested the hypothesis that surveillance neuroimaging and neurologic examinations identified changes requiring emergent surgical interventions in patients with intracerebral hemorrhage (ICH). Methods: Patients with primary ICH were enrolled into a prospective registry between December 2006 and July 2012. Patients were managed in a neuroscience intensive care unit with a protocol that included serial neuroimaging at 6, 24, and 48 hours, and hourly neurologic examinations using the Glasgow Coma Scale and NIH Stroke Scale. We evaluated all cases of craniotomy and ventriculostomy to determine whether the procedure was part of the initial management plan or occurred subsequently. For those that occurred subsequently, we determined whether worsening on neurologic examination or worsened neuroimaging findings initiated the process leading to intervention. Results: There were 88 surgical interventions in 84 (35%) of the 239 patients studied, including ventriculostomy in 52 (59%), craniotomy in 21 (24%), and both in 11 (13%). Of the 88 interventions, 24 (27%) occurred subsequently and distinctly from initial management, a median of 15.9 hours (8.9–27.0 hours) after symptom onset. Thirteen (54%) were instigated by findings on neurologic examination and 11 (46%) by neuroimaging. Demographics, severity of hemorrhage, and hemorrhage location were not associated with delayed intervention. Conclusions: More than 25% of surgical interventions performed after ICH were prompted by delayed imaging or clinical findings. Serial neurologic examinations and neuroimaging are important and effective surveillance techniques for monitoring patients with ICH.

Predictors of 30-day readmission after intracerebral hemorrhage: a single-center approach for identifying potentially modifiable associations with readmission.

Objective:To determine whether patient’s demographics or severity of illness predict hospital readmission within 30 days following spontaneous intracerebral hemorrhage, to identify readmission associations that may be modifiable at the single-center level, and to determine the impact of readmission on outcomes. Design:We collected demographic, clinical, and hospital course data for consecutive patients with spontaneous intracerebral hemorrhage enrolled in an observational study. Readmission within 30 days was determined retrospectively by an automated query with manual confirmation. We identified the reason for readmission and tested for associations between readmission and functional outcomes using modified Rankin Scale (a validated functional outcome measure from 0, no symptoms, to 6, death) scores before intracerebral hemorrhage and at 14 days, 28 days, and 3 months after intracerebral hemorrhage. Setting:Neurologic ICU of a tertiary care hospital. Patients:Critically ill patients with spontaneous intracerebral hemorrhage. Interventions:Patients received standard critical care management for intracerebral hemorrhage. Measurements and Main Results:Of 246 patients (mean age, 65 yr; 51% female), 193 patients (78%) survived to discharge. Of these, 22 patients (11%) were readmitted at a median of 9 days (interquartile range, 4–15 d). The most common readmission diagnoses were infections after discharge (n = 10) and vascular events (n = 6). Age, history of stroke and hypertension, severity of neurologic deficit at admission, Acute Physiology and Chronic Health Evaluation score, ICU and hospital length of stay, ventilator-free days, days febrile, and surgical procedures were not predictors of readmission. History of coronary artery disease was associated with readmission (p = 0.03). Readmitted patients had similar modified Rankin Scale and severity of neurologic deficit at 14 days but higher (worse) modified Rankin Scale scores at 3 months (median [interquartile range], 5 [3–6] vs 3 [1–4]; p = 0.01). Conclusions:Severity of illness and hospital complications were not associated with 30-day readmission. The most common indication for readmission was infection after discharge, and readmission was associated with worse functional outcomes at 3 months. Preventing readmission after intracerebral hemorrhage may depend primarily on optimizing care after discharge and may improve functional outcomes at 3 months.

Subarachnoid Extension of Primary Intracerebral Hemorrhage is Associated With Poor Outcomes

Background and Purpose— Extension of hemorrhage into the subarachnoid space is observed in primary intracerebral hemorrhage (ICH), yet the phenomenon has undergone limited study and is of unknown significance. The objective of this study is to evaluate the incidence, characteristics, and clinical consequences of subarachnoid hemorrhage extension (SAHE) in ICH on functional outcomes. Methods— Patients with primary ICH were enrolled into a prospective registry between December 2006 and June 2012. Patients were managed and serial neuroimaging was obtained per a structured protocol. Presence of any subarachnoid blood on imaging was identified as SAHE by expert reviewers blinded to outcomes. Regression models were developed to test whether the occurrence of SAHE was an independent predictor of functional outcomes as measured with the modified Rankin Scale. Results— Of 234 patients with ICH, 93 (39.7%) had SAHE. Interrater agreement for SAHE was excellent (kappa=0.991). SAHE was associated with lobar hemorrhage location (65% of SAHE vs 19% of non-SAHE cases; P<0.001) and larger hematoma volumes (median 23.8 vs 6.7; P<0.001). Fever (69.9% vs 51.1%; P=0.005) and seizures (8.6% vs 2.8%; P=0.07) were more common in patients with SAHE. SAHE was a predictor of death by day 14 (odds ratio, 4.45; 95% confidence interval, 1.88–10.53; P=0.001) and of higher (worse) modified Rankin Scale scores at 28 days (odds ratio, 1.76 per mRS point; 95% confidence interval, 1.01–3.05; P=0.012) after adjustment for ICH score. Conclusions— SAHE is associated with worse modified Rankin Scale independent of traditional ICH severity measures. Underlying mechanisms and potential treatments of SAHE require further study.

Magnetic resonance imaging versus computed tomography for identification and quantification of intraventricular hemorrhage.

BACKGROUND Intraventricular hemorrhage (IVH) may be difficult to detect especially when in small amounts and may affect outcomes. The objective of this study was to compare the sensitivity of magnetic resonance imaging (MRI) vs computed tomography (CT) for the identification and quantification of IVH. METHODS Patients with primary intracerebral hemorrhage were enrolled into a prospective registry between December 2006 and June 2013. Diagnostic and surveillance neuroimaging studies were analyzed for the presence of IVH and quantified by Graeb score. In subjects who developed IVH and underwent both MRI and CT, each MRI was paired with the CT scan done at the closest time point, and Graeb scores were compared with the Wilcoxon signed rank test for related samples. RESULTS There were 289 subjects in the cohort with IVH found in 171. Sixty-eight pairs of MRI and CT were available for comparison. CT failed to detect IVH in 3% of cases, whereas MRI was 100% sensitive. MRI and CT yielded equal Graeb scores in 72% of the pairs, and MRI Graeb score was higher in 24% (P = .007). CONCLUSIONS MRI identifies small volumes of IVH in cases not detected by CT and yields higher estimates of intraventricular blood volume. These data indicate that consideration of technical differences is needed when comparing images from the 2 modalities in the evaluation for IVH.

Subarachnoid extension of hemorrhage is associated with early seizures in primary intracerebral hemorrhage.

BACKGROUND Seizures are common in patients with subarachnoid hemorrhage, potentially by inciting cortical irritability. Seizures are also commonly seen after intracerebral hemorrhage (ICH), although the mechanisms and risk factors within that population are not well understood. The objective of this study is to evaluate whether subarachnoid hemorrhage extension (SAHE) is associated with early seizures in patients with primary ICH. METHODS Patients with primary ICH were enrolled into a prospective registry between December 2006 and July 2012. Patients were managed per a structured protocol. SAHE was identified on imaging by expert reviewers blinded to outcomes. Electroencephalograms were routinely obtained in patients with unexplained, poor level of arousal. Seizure was determined by clinically observed convulsions or traditional electroencephalographic criteria. Early seizures were defined as occurring within 3 days of hemorrhage. A binary logistic regression model was developed to test whether the occurrence of SAHE was independently associated with seizures. RESULTS A total of 234 patients were studied. Of these, 93 (40%) had SAHE and 9 (4%) had early seizures. SAHE was associated with early seizures (P = .03). No additional variables were identified by regression modeling to mediate the association between SAHE and early seizures (odds ratio 5.62 [95% confidence interval 1.14-27.7], P = .034). CONCLUSIONS SAHE is associated with early seizures in patients with primary ICH. Further study is needed to confirm these findings and determine whether modifications to routine care based on the presence of SAHE would be of benefit.

Pearls & Oy-sters: Bilateral thalamic involvement in West Nile virus encephalitis

Bilateral thalamic inflammation in the presence of a clinical picture suggestive of viral encephalitis should raise concern for West Nile virus infection.

Preadmission statin use does not improve functional outcomes or prevent delayed ischemic events in patients with spontaneous subarachnoid hemorrhage.

To determine whether preadmission statin use in patients with spontaneous subarachnoid hemorrhage (SAH) is associated with improved functional outcomes and a lower incidence of delayed cerebral ischemic events compared with statin‐naive patients with SAH.

23.4% Saline Decreases Brain Tissue Volume in Severe Hepatic Encephalopathy as Assessed by a Quantitative CT Marker.

Objective:Cerebral edema is common in severe hepatic encephalopathy and may be life threatening. Bolus 23.4% hypertonic saline improves surveillance neuromonitoring scores, although its mechanism of action is not clearly established. We investigated the hypothesis that bolus hypertonic saline decreases cerebral edema in severe hepatic encephalopathy utilizing a quantitative technique to measure brain and cerebrospinal fluid volume changes. Design:Retrospective analysis of serial CT scans, and clinical data for a case-control series were performed. Setting:ICUs of a tertiary care hospital. Patients:Patients with severe hepatic encephalopathy treated with 23.4% hypertonic saline and control patients who did not receive 23.4% hypertonic saline. Interventions:23.4% hypertonic saline bolus administration. Measurements and Main Results:We used clinically obtained CT scans to measure volumes of the ventricles, intracranial cerebrospinal fluid, and brain using a previously validated semiautomated technique (Analyze Direct, Overland Park, KS). Volumes before and after 23.4% hypertonic saline were compared with Wilcoxon signed rank test. Associations among total cerebrospinal fluid volume, ventricular volume, serum sodium, and Glasgow Coma Scale scores were assessed using Spearman rank correlation test. Eleven patients with 18 administrations of 23.4% hypertonic saline met inclusion criteria. Total cerebrospinal fluid (median, 47.6 mL [35.1–69.4 mL] to 61.9 mL [47.7–87.0 mL]; p < 0.001) and ventricular volumes (median, 8.0 mL [6.9–9.5 mL] to 9.2 mL [7.8–11.9 mL]; p = 0.002) increased and Glasgow Coma Scale scores improved (median, 4 [3–6] to 7 [6–9]; p = 0.008) after 23.4% hypertonic saline. In contrast, total cerebrospinal fluid and ventricular volumes decreased in untreated control patients. Serum sodium increase was associated with increase in total cerebrospinal fluid volume (r = 0.83, p < 0.001), and change in total cerebrospinal fluid volume was associated with ventricular volume change (r = 0.86; p < 0.001). Conclusions:Total cerebrospinal fluid and ventricular volumes increased after 23.4% hypertonic saline, consistent with a reduction in brain tissue volume. Total cerebrospinal fluid and ventricular volume change may be useful quantitative measures to assess cerebral edema in severe hepatic encephalopathy.

Acute changes in ventricular volume during treatment for hepatic and renal failure.

Hepatic encephalopathy (HE) exists on a spectrum from minimal dysfunction to coma and may arise from ammonia-associated neurotoxicity whereby metabolic dysfunction leads to glutamine accumulation, astrocyte swelling, and nitric oxide–induced vasodilation.1 Elevated intracranial pressure (ICP), secondary to cerebral edema, is common in liver failure and occurs in 80% of comatose patients.1–3 Nonetheless, invasive ICP monitoring remains contentious in HE due to hemorrhagic complications and lack of evidence supporting benefit.3 A radiographic technique to assess edema could be helpful but head CT is only 33% sensitive for cerebral edema.2,3 We present a case illustrating this limitation of CT, the potential for rapid changes in cerebral edema, and a potential noninvasive means of assessing cerebral edema evolution.