INTRODUCTION:Inguinal hernia repair is a common surgical procedure, and effective post-operative pain management is crucial for patient recovery. This study compares the efficacy of laparoscopic-guided transversus abdominis plane (LTAP) block and port-site local anaesthetic infiltration (PSLAI) in post-operative pain relief after laparoscopic transabdominal preperitoneal (TAPP) inguinal hernia repair. This study was done to evaluate the effectiveness of LTAP versus PSLAI in controlling post-operative pain, reducing hospital stay duration and accelerating recovery following TAPP inguinal hernia repair. PATIENTS AND METHODS:A randomised controlled trial was conducted with 60 patients, divided into two groups: LTAP and PSLAI. Pain levels were measured using the Visual Analogue Scale at 6, 12, 24 h and at discharge. The need for rescue analgesia, hospital stay duration and time to return to normal activities were also assessed. RESULTS:The LTAP group showed significantly lower pain scores at all post-operative time points compared to the PSLAI group (P values from 0.0017 to 0.0154). In addition, the LTAP group had a significantly shorter hospital stay (P = 0.0002) and quicker return to daily activities (P = 0.002). The need for rescue analgesia was significantly lower in the LTAP group (P = 0.043). CONCLUSION:LTAP block provided superior pain relief, reduced hospital stays and facilitated faster recovery compared to PSLAI. This technique should be considered for enhanced post-operative management following TAPP inguinal hernia repair.

Background Baseline anemia is associated with poor intracerebral hemorrhage (ICH) outcomes. However, underlying drivers for anemia and whether anemia development after ICH impacts clinical outcomes are unknown. We hypothesized that inflammation drives anemia development after ICH and assessed their relationship to outcomes. Methods and Results Patients with serial hemoglobin and iron biomarker concentrations from the HIDEF (High‐Dose Deferoxamine in Intracerebral Hemorrhage) trial were analyzed. Adjusted linear mixed models assessed laboratory changes over time. Of 42 patients, significant decrements in hemoglobin occurred with anemia increasing from 19% to 45% by day 5. Anemia of inflammation iron biomarker criteria was met in 88%. A separate cohort of 521 patients with ICH with more granular serial hemoglobin and long‐term neurological outcome data was also investigated. Separate regression models assessed whether (1) systemic inflammatory response syndrome (SIRS) scores related to hemoglobin changes over time and (2) hemoglobin changes related to poor 90‐day outcome. In this cohort, anemia prevalence increased from 30% to 71% within 2 days of admission yet persisted beyond this time. Elevated systemic inflammatory response syndrome was associated with greater hemoglobin decrements over time (adjusted parameter estimate: −0.27 [95% CI, −0.37 to −0.17]) and greater hemoglobin decrements were associated with poor outcomes (adjusted odds ratio per 1 g/dL increase, 0.76 [95% CI, 0.62–0.93]) independent to inflammation and ICH severity. Conclusions We identified novel findings that acute anemia development after ICH is common, rapid, and related to inflammation. Because anemia development is associated with poor outcomes, further work is required to clarify if anemia, or its underlying drivers, are modifiable treatment targets that can improve ICH outcomes. Registration https://www.clinicaltrials.gov Unique identifier: NCT01662895

Anemic intracerebral hemorrhage (ICH) patients are observed to have poor clinical outcomes with increased risk of hematoma expansion (HE) and impaired cerebral oxygenation. To assess whether anemia causes these observations, we assessed neuroimaging evidence of HE and neuropathological changes of hypoxia and blood brain barrier (BBB) dysfunction in anemic vs non-anemic mice with ICH. Anemia was generated in 3 month old female C57/BL6 mice using iron-deficient chow. Age and sex-matched controls were fed iron-replete control diet. Anemia was verified using modified Drabkin assays. Collagenase was used to induce ICH. ICH volume and HE were quantified using serial T2-weighed MRI at 1, 4, and 24 hours after ICH. Early 24 hour mortality was recorded. After the last MRI, surviving mice were euthanized by intracardiac perfusion and the brain was processed for histological analysis of vascular permeability (IgG), microglia number and activation (Iba1 and CD68), and response to hypoxia (HIF1α). Statistical analyses were performed using two-tailed ANOVA. Compared to controls, anemic mice displayed larger final ICH lesion volumes (anemia: 7.7 mm 3 vs control: 6.1 mm 3 ), greater HE at 24 hours (anemia: 111.4% vs control: 23.6%) and increased early mortality (anemia: 30% vs control: 0%). Histological analyses revealed that, while microglial activation and BBB permeability to serum IgGs in control mice were restricted to the ipsilateral hemisphere and mostly localized perilesionally, anemic mice had increased immune infiltration and increased BBB permeability in both hemispheres. Similarly, non-ICH anemic mice showed increased and widespread immune cell infiltration and increased BBB permeability compared to non-ICH control mice, suggesting that consistently low hemoglobin concentrations may increase cerebrovascular susceptibility to injury.Future studies will be needed to further clarify cellular and molecular mechanisms driving our findings and whether anemia can be a treatable target to improve ICH outcomes.

Background: Ischemic lesions on diffusion weighted imaging (DWI) occur in one-third of intracerebral hemorrhage (ICH). Due to conflicting prior studies, it is uncertain if the degree of systolic blood pressure reduction increases the risk. Patients with severe, chronic hypertension may be more vulnerable to the development of ischemia after ICH due to altered cerebral autoregulatory limits. Using cardiac remodeling as a biomarker for severe chronic hypertension, we hypothesized that the presence of left ventricular hypertrophy (LVH) is associated with DWI lesions. Methods: Patients with spontaneous ICH enrolled in the Intracerebral Hemorrhage Outcomes Project who underwent DWI imaging and transthoracic echocardiography (TTE) during hospitalization were included. Lesions were identified as hyperintensities >10mm remote from the hematoma with corresponding low ADC signal. LVH presence was identified using clinically obtained TTE reports with imaging evidence of moderate-severe left ventricular wall thickness. The relationship between LVH and DWI ischemic lesions was assessed with logistic regression modeling after adjusting for age, ICH volume, intraventricular hemorrhage, hypertension history, and blood pressure change within 24 hours. A secondary analysis using linear regression assessed the association with the number of DWI lesions adjusting for similar covariates. Results: Of 187 patients analyzed, DWI lesions were observed in 30.5% and LVH was seen in 23.5%. In our logistic regression analyses, we identified that LVH was associated with DWI lesions (adjusted OR 2.77, CI: 1.19-6.40). Separate sensitivity analyses adjusting for sex (OR 2.47, CI 1.05-5.83) and race (OR 2.52, CI 1.08-5.91) did not change these relationships. In secondary analysis, we identified that LVH was associated with increased DWI lesion number (B 1.018, CI 0.40-1.63 ). Discussion: LVH is associated with the presence and burden of DWI lesions. Further work is required to assess aggregate relationships of chronic hypertension/LVH, acute blood pressure change, ischemic lesions, and ICH outcomes to determine whether patients with LVH necessitate different acute blood pressure treatment goals.

Background: We have previously identified that hemoglobin decrements and new-onset anemia during an intracerebral hemorrhage (ICH) hospitalization is frequent, rapid, and associates with poor outcome. Though this association may be related to impaired cerebral oxygen delivery, it is unclear whether these changes relate to cerebral ischemia. We investigated the relationship of hemoglobin decrements over time and ischemic lesions on brain MRI during an ICH hospitalization. Methods: Consecutive patients with acute spontaneous ICH enrolled into a single-center, prospective cohort study between 2009 and 2019 were assessed. Patients who had a brain MRI and serial hemoglobin measurements were included. Change in hemoglobin from admission to date of brain MRI (delta Hgb) was defined as the exposure. The outcome was the presence of remote ischemic lesions, defined as foci of diffusion restriction >10 mm away from the hematoma on brain MRI. A regression model assessed relationships between delta Hgb and DWI brain lesions, adjusting for baseline demographics, ICH severity, and time to MRI. Separate sensitivity models were adjusted for admission systolic blood pressure and hemoglobin. Results: We identified 189 ICH patients with brain MRI and serial hemoglobin measurements during their hospitalization. The mean age was 66.5 (SD 14.8) and 49.2% were female. Mean admission hemoglobin was 13.5 g/dL (SD 2.0), mean change in hemoglobin from admission to day of MRI was -1.6 (SD 1.6), median time from ICH onset to MRI was 2 (IQR 1-4) days, and 31.7% of patients had ischemic lesions on MRI. We identified an association of greater decrements in hemoglobin with ischemic lesions in our primary model (adjusted OR 0.79, 95%CI 0.64-0.99, p=0.04). Sensitivity analyses adjusting for admission systolic blood pressure and hemoglobin did not change this association. Conclusions: Greater hemoglobin decrements associate with remote ischemic lesions on brain MRI of patients with acute ICH. Further work is needed to assess drivers of anemia after ICH and possible causal mechanisms for ischemic brain injury to assess whether anemia is a modifiable treatment target to improve ICH outcomes.

BACKGROUND: Hypoperfusion due to blood pressure (BP) reduction is a potential mechanism of cerebral ischemia after intracerebral hemorrhage. However, prior evaluations of the relationship between BP reduction and ischemia have been conflicting. Untreated chronic hypertension is common in intracerebral hemorrhage and alters cerebral autoregulation. We hypothesized that the risk of diffusion-weighted imaging (DWI) hyperintensities from acute BP reduction is modified by premorbid BP control. METHODS: Individuals enrolled in the ERICH study (Ethnic/Racial Variations of Intracerebral Hemorrhage) from 2010 to 2015 were categorized as untreated, treated, or nonhypertensive based on preintracerebral hemorrhage diagnosis and antihypertensive medication use. The percent reduction of systolic BP (SBP) was calculated between presentation and 24 hours from admission. The primary outcome was the presence of DWI lesions. Using logistic regression, we tested the association between chronic hypertension status, SBP reduction, and their interaction with DWI lesion presence. RESULTS: From 3000 participants, 877 with available magnetic resonance imaging met inclusion (mean age, 60.5±13.3 years; 42.5% women). DWI lesions were detected in 25.9%. Untreated, treated, and no hypertension accounted for 32.6%, 47.9%, and 19.5% of cases, respectively. SBP reduction was not directly associated with DWI lesions; however, an interaction effect was observed between SBP reduction and chronic hypertension status ( P =0.036). Nonhypertensive subjects demonstrated a linear risk of DWI lesion presence with greater SBP reduction, whereas untreated hypertension demonstrated a stable risk across a wide range of SBP reduction ( P =0.023). CONCLUSIONS: Premorbid BP control, especially untreated hypertension, may influence the relationship between DWI lesions and acute BP reduction after intracerebral hemorrhage. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01202864.

Background: Ischemia on diffusion weighted imaging (DWI) after intracerebral hemorrhage (ICH) increases the risk of future ischemic stroke. Radiographic markers of small vessel disease, including cerebral microbleeds (CMB), are associated with DWI lesions. Though cortical superficial siderosis (cSS) is also a hemorrhagic small vessel disease subtype, it is unclear if cSS similarly relates to DWI lesions. We hypothesized that cSS would represent a more severe phenotype of small vessel disease and would associate with DWI lesions after ICH independent to other small vessel disease markers. Methods: Using the Intracerebral Hemorrhage Outcomes Project (ICHOP), we included all cases of spontaneous ICH who underwent DWI and susceptibility imaging/gradient echo. DWI hyperintensities were identified if >10mm from the hematoma with decreased ADC signal. cSS were identified as subarachnoid hemosiderin deposition without acute subarachnoid hemorrhage. The relationship of cSS with DWI lesion presence as the outcome was assessed with logistic regression adjusted for ICH score, blood pressure change within 24 hours, and small vessel disease markers (CMB and white matter hyperintensity). Sensitivity analyses were performed to adjust for demographics and ICH location. A secondary analysis using linear regression assessed the association with the number of DWI lesions adjusted for similar covariates. Results: Of 198 patients analyzed, DWI lesions were observed in 31.3% and cSS in 10.6%. The presence of cSS was associated with DWI lesions (adjusted OR 3.72, CI: 1.29-10.72), independent of other small vessel disease markers. Separate sensitivity analyses adjusting for sex, race, and ICH location did not change the association of cSS with DWI lesions. In secondary analyses, cSS was not associated with greater number of DWI lesions counts (b 0.213, CI -0.53-0.63). Discussion: cSS is associated with the presence of DWI lesions, independent to other small vessel disease markers. cSS may represent a severe phenotype of small vessel disease with a risk of ICH recurrence and ischemia. Further work is required to investigate underlying mechanisms and optimal strategies to mitigate competing risks of future hemorrhage and ischemic events in these patients.

Abstract Introduction Acute internal carotid artery (ICA) occlusions have a precise differential, of which includes Eagle’s Syndrome, which is due to disfigured or elongated styloid processes. This can result in 1) unilateral oropharyngeal, facial and auricular pain due to irritation of the glossopharyngeal nerve or 2) carotid artery dissection. In this report, we highlight the diagnostic/management approach to the latter. Case Presentation A 51-year-old man presented with acute onset aphasia and right sided weakness, was found to have a L ICA occlusion and on further review to have a R ICA occlusion in the past. Ultimately, workup was consistent with bilateral carotid artery dissections – Eagle’s Syndrome. Conclusions Bilateral Eagle’s Syndrome is an extremely care condition, and this case report highlights the diagnostic/management considerations, especially as it relates to the utilization of multiple imaging modalities.

The NOAA/NASA Fire Influence on Regional to Global Environments and Air Quality (FIREX-AQ) experiment was a multi-agency, inter-disciplinary research effort to: (a) obtain detailed measurements of trace gas and aerosol emissions from wildfires and prescribed fires using aircraft, satellites and ground-based instruments, (b) make extensive suborbital remote sensing measurements of fire dynamics, (c) assess local, regional, and global modeling of fires, and (d) strengthen connections to observables on the ground such as fuels and fuel consumption and satellite products such as burned area and fire radiative power. From Boise, ID western wildfires were studied with the NASA DC-8 and two NOAA Twin Otter aircraft. The high-altitude NASA ER-2 was deployed from Palmdale, CA to observe some of these fires in conjunction with satellite overpasses and the other aircraft. Further research was conducted on three mobile laboratories and ground sites, and 17 different modeling forecast and analyses products for fire, fuels and air quality and climate implications. From Salina, KS the DC-8 investigated 87 smaller fires in the Southeast with remote and in-situ data collection. Sampling by all platforms was designed to measure emissions of trace gases and aerosols with multiple transects to capture the chemical transformation of these emissions and perform remote sensing observations of fire and smoke plumes under day and night conditions. The emissions were linked to fuels consumed and fire radiative power using orbital and suborbital remote sensing observations collected during overflights of the fires and smoke plumes and ground sampling of fuels. Plain Language Summary The NOAA/NASA Fire Influence on Regional to Global Environments and Air Quality (FIREX-AQ) experiment was aimed at understanding how fuel and fire conditions at the point of emission influence the chemistry of smoke, what conditions and processes control the rise of smoke plumes, what happens to smoke as it is distributed in the atmosphere, and how chemical transformation of smoke impacts air quality, weather, and climate downwind. Lessons learned from FIREX-AQ will also be used to assess and improve the effectiveness of satellites for estimating the emissions from wildfires and prescribed burns and to reduce uncertainties associated with modeling and forecasting of smoke. Here we present an overview of the FIREX-AQ effort, its motivation and design, with detailed descriptions of the measurements and analyses carried out, their connections to FIREX-AQ science goals, and the early findings of this exceptionally broad effort to understand fire and its many impacts on the atmosphere.

Introduction: Hemoglobin concentrations and diffusion weighted imaging (DWI) lesions are separately known to be associated with poor intracerebral hemorrhage (ICH) outcomes. Though hemoglobin concentrations are related to both hypoxia and thrombosis at their extremes, it is unknown whether hemoglobin concentrations relate to DWI lesions after ICH. Methods: Spontaneous, supratentorial ICH patients with available baseline hemoglobin and hospitalized MRI data enrolled into a multicenter cohort study between 2010-2016 were analyzed. Baseline hemoglobin was assessed as both a continuous variable (g/dL) and categorical variable (<11, 11 to <13, 13 to <15, >/=15 g/dL). Primary analyses assessed relationships of baseline hemoglobin with MRI DWI lesions. Secondary analyses assessed independent relationships of hemoglobin and DWI lesions with poor 3-month outcomes (modified Rankin Scale [mRS] 4-6). Separate multivariable regression models assessed these relationships after adjusting for relevant covariates. Results: Of 917 ICH patients analyzed, the mean baseline hemoglobin was 13.8 g/dL (+/-1.9), 60% were deep ICH, and DWI lesions were identified in 27% of the cohort. In our primary analyses, increased hemoglobin, defined as a continuous variable, was associated with DWI lesions (adjusted OR 1.21, 95% CI: 1.07-1.37) after adjusting for sex, race, ICH severity, time to MRI, and blood pressure treatment change. In secondary analyses, DWI lesions were associated with poor 3-month outcomes (adjusted OR 1.83, 95% CI: 1.24-2.69) adjusting for similar covariates. We identified associations of low hemoglobin categories, when referenced to hemoglobin 13 to <15 g/dL, with poor outcomes (<11 g/dL: adjusted OR 1.99, 95% CI: 1.05-3.79; 11 to <13 g/dL: adjusted OR 1.62, 95% CI: 1.04-2.52). Effect estimates of high hemoglobin (>/=15 g/dL) with poor outcomes were smaller and imprecise (adjusted OR 1.39, 95% CI: 0.89-2.17). Conclusions: We identified novel relationships between higher baseline hemoglobin concentrations and DWI lesions in ICH patients. Further studies are required to clarify the role of hemoglobin concentrations on both cerebral small vessel disease pathophysiology and ICH outcomes.

OBJECTIVES: Low hemoglobin concentration impairs clinical hemostasis across several diseases. It is unclear whether hemoglobin impacts laboratory functional coagulation assessments. We evaluated the relationship of hemoglobin concentration on viscoelastic hemostatic assays in intracerebral hemorrhage (ICH) and perioperative patients admitted to an ICU. DESIGN: Observational cohort study and separate in vitro laboratory study. SETTING: Multicenter tertiary referral ICUs. PATIENTS: Two acute ICH cohorts receiving distinct testing modalities: rotational thromboelastometry (ROTEM) and thromboelastography (TEG), and a third surgical ICU cohort receiving ROTEM were evaluated to assess the generalizability of findings across disease processes and testing platforms. A separate in vitro ROTEM laboratory study was performed utilizing ICH patient blood samples. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Relationships between baseline hemoglobin and ROTEM/TEG results were separately assessed across patient cohorts using Spearman correlations and linear regression models. A separate in vitro study assessed ROTEM tracing changes after serial hemoglobin modifications from ICH patient blood samples. In both our ROTEM ( n = 34) and TEG ( n = 239) ICH cohorts, hemoglobin concentrations directly correlated with coagulation kinetics (ROTEM r : 0.46; p = 0.01; TEG r : 0.49; p < 0.0001) and inversely correlated with clot strength (ROTEM r : –0.52, p = 0.002; TEG r : –0.40, p < 0.0001). Similar relationships were identified in perioperative ICU admitted patients ( n = 121). We continued to identify these relationships in linear regression models. When manipulating ICH patient blood samples to achieve lower hemoglobin concentrations in vitro, we similarly identified that lower hemoglobin concentrations resulted in progressively faster coagulation kinetics and greater clot strength on ROTEM tracings. CONCLUSIONS: Lower hemoglobin concentrations have a consistent, measurable impact on ROTEM/TEG testing in ICU admitted patients, which appear to be artifactual. It is possible that patients with low hemoglobin may appear to have normal viscoelastic parameters when, in fact, they have a mild hypocoagulable state. Further work is required to determine if these tests should be corrected for a patient’s hemoglobin concentration.

Background: We identified that major ABO incompatible platelet transfusions are associated with poor intracerebral hemorrhage (ICH) outcomes, yet the driver for this relationship is unknown and does not appear to be related to impaired hemostasis. Conversely, acute ICH patients are known to develop remote ischemic lesions on brain MRI. These ischemic lesions are associated with poor ICH outcomes, but risk factors for their formation are unknown. We explored whether major ABO incompatible platelet transfusions are associated with these ischemic lesions. Methods: Consecutive spontaneous ICH patients enrolled into a single-center, prospective cohort study between 2009 and 2016 were assessed. Patients receiving an acute, single platelet transfusion within 24 h of admission and a brain MRI during their ICH admission were included. Major ABO incompatible platelet transfusion was the exposure. The presence of ischemic lesions on brain MRI, defined as diffusion restriction >10 mm away from the hematoma was the outcome. Regression models assessed relationships between major ABO-incompatible platelets and ischemic lesions, adjusting for ICH severity and time to MRI. Results: Of 40 ICH patients with an acute platelet transfusion and MRI, the mean age was 67.1 (SD 14.1), 37.5% were female, and 20% received a major ABO incompatible platelet unit. Patients receiving a major incompatible platelet unit were more likely to have ischemic lesions (62.5% vs 21.9%), and there continued to be an association of major ABO-incompatible platelets units with these lesions after adjusting for time to MRI (OR 5.45, 95%CI 1.01-29.30, p=0.04) and ICH score (OR 9.15, 95%CI 1.37-62.67, p=0.02). Sensitivity analyses adjusting for patient blood type did not alter this relationship (OR 17.08, 95%CI 1.34-217.94, p = 0.03). Conclusions: Major ABO incompatible platelet units were associated with remote ischemic DWI lesions. Further work is needed to address the generalizability of our data and to clarify relationships of platelet unit characteristics, cerebral ischemia, and clinical outcomes after ICH.

Introduction: Low hemoglobin is associated with stroke and poor cerebrovascular outcomes. It is unclear whether hemoglobin concentrations directly impact cerebrovascular health. Thus, we sought to investigate the role of hemoglobin concentration on cerebral hypoxia and blood brain barrier (BBB) function in murine models of anemia. Hypothesis: Low hemoglobin will cause relevant cerebral hypoxic changes and impair BBB function. Methods: Two different models of anemia and their respective controls were generated from 30 8-week-old, female C57/BL6 mice. The separate cohorts generated included: 1) an acute anemia model cohort via anti-TER119 injection (red blood cell hemolysis) compared to IgG control injected mice; 2) chronic anemia model cohort via iron-deficient chow compared to iron replete diet control. Hemoglobin concentrations were assessed using modified Drabkin assays. Mice were euthanized by intracardiac perfusion with saline and fixative and the brain was dissected and processed for histological analysis of vascular permeability (IgG), microglia number and activation (Iba1 and CD68), response to hypoxia (HIF1α) and endothelial markers of BBB function (GLUT1). Statistical analyses were performed using two-tailed Student's t-tests. Results: Hemoglobin concentrations were lower in our separate anemia model mice compared to their respective controls (acute anemia: 5.5 ± 4.02 vs 13.1 ± 1.69, p=0.007; chronic anemia: 7.9 ± 1.05 vs 11.9 ± 2.31, p=0.0006). Postmortem histological analyses revealed stronger microglial activation (p<0.005) and higher microglial expression of hypoxia-response protein HIF1α (p<0.05) in both acute and chronic anemia models compared to their respective controls. Additionally, anemic mice had increased vascular permeability to serum IgG and decreased expression of the endothelial-specific glucose transporter GLUT1 (p<0.05). Conclusions: Anemic mice appear to display stronger microglial activation, greater HIF1α expression, and BBB dysfunction compared to non-anemic mice. Future studies will be needed to further clarify cellular and molecular mechanisms driving relationships between anemia, hypoxia, BBB dysfunction and clinical outcomes in cerebrovascular disease.

Introduction: Following intracerebral hemorrhage (ICH), elevated cerebral tissue iron concentrations are seen. It is unclear how peripheral serum iron concentrations change over time and how they relate to anemia after ICH. Given the known impacts of iron concentrations and anemia on clinical outcomes, we explored serum iron biomarker and hemoglobin concentration changes after acute ICH. Methods: A post hoc analysis of patients with available serial (baseline and 5 day) serum biomarker data from the multicenter, High Dose Deferoxamine in Intracerebral Hemorrhage (HI-DEF) trial was performed. Changes of serum hemoglobin, iron, transferrin, and ferritin were assessed using repeated measure ANOVA analyses. Deferoxamine treatment and poor 90 day modified Rankin Scale 4-6 were separately assessed as between subject factors for these laboratory changes. Results: Of 42 ICH patients analyzed, the mean age was 64, 62% were male, median ICH volume was 15.7mL (IQR 5.7-37.5), and baseline anemia was seen in 19%. We identified significant decrements of hemoglobin (mean difference -1.4 g/dL; 95%CI: -1.9 to -0.9; p<0.0001), iron (mean difference -16.9 ug/dL; 95%CI: -29.7 to -4.1; p=0.01), transferrin (mean difference -43.9 ng/mL; 95%CI: -56.6 to -31.3; p<0.0001), and conversely, significant ferritin elevations (mean difference 104.5 ug/L; 95%CI: 52.5-156.6; p<0.0001) at 5 days. Anemia was identified in 43% of patients at 5 days. Deferoxamine did not have a significant impact on these repeated measures. Patients with poor long-term outcomes had greater decrements in hemoglobin compared to those with good outcomes (mean difference: -1.5 g/dL; 95%CI: -2.6 to -0.3; p=0.01). Conclusions: Serum iron and hemoglobin concentrations decrease significantly over time following ICH. Patients with worse long term ICH outcomes had greater hemoglobin decrements during their hospitalization. The aggregate iron biomarker and hemoglobin concentration changes suggest anemia development may be due to anemia of inflammation. Further work is required to address the pathophysiologic difference between systemic and central iron homeostasis mechanisms following ICH and the impacts that ICH has on inflammation, systemic iron homeostasis, anemia, and clinical outcomes.

Assessments of consciousness are a critical part of prognostic algorithms for critically ill patients suffering from severe brain injuries. There have been significant advances in the field of coma science over the past two decades, providing clinicians with more advanced and precise tools for diagnosing and prognosticating disorders of consciousness (DoC). Advanced neuroimaging and electrophysiological techniques have vastly expanded our understanding of the biological mechanisms underlying consciousness, and have helped identify new states of consciousness. One of these, termed cognitive motor dissociation, can predict functional recovery at 1 year post brain injury, and is present in up to 15-20% of patients with DoC. In this chapter, we review several tools that are used to predict DoC, describing their strengths and limitations, from the neurological examination to advanced imaging and electrophysiologic techniques. We also describe multimodal assessment paradigms that can be used to identify covert consciousness and thus help recognize patients with the potential for future recovery and improve our prognostication practices.

Background: Hemoglobin concentration and diffusion-weighted imaging (DWI) ischemic lesions are separately known to be associated with poor intracerebral hemorrhage (ICH) outcomes. While hemoglobin concentrations have known relationships with ischemic stroke, it is unclear whether hemoglobin concentration is associated with DWI ischemic lesions after ICH. We sought to investigate the hypothesis that hemoglobin concentrations would associate with DWI lesions after ICH and further investigated their relationships with clinical outcomes. Methods: Supratentorial ICH patients enrolled between 2010 and 2016 to a prospective, multicenter, observational cohort study (ERICH study [Ethnic/Racial Variations of Intracerebral Hemorrhage]) were assessed. Patients from this study with baseline, admission hemoglobin, and hospitalization magnetic resonance imaging were analyzed. Hemoglobin was examined as the primary exposure variable defined as a continuous variable (g/dL). Magnetic resonance imaging DWI ischemic lesion presence was assessed as the primary radiographic outcome. Primary analyses assessed relationships of hemoglobin with DWI lesions. Secondary analyses assessed relationships of DWI lesions with poor 3-month outcomes (modified Rankin Scale score, 4–6). These analyses were performed using separate multivariable logistic regression models adjusting for relevant covariates. Results: Of 917 patients with ICH analyzed, mean baseline hemoglobin was 13.8 g/dL (±1.9), 60% were deep ICH, and DWI lesions were identified in 27% of the cohort. In our primary analyses, increased hemoglobin, defined as a continuous variable, was associated with DWI lesions (adjusted odds ratio, 1.21 per 1 g/dL change in hemoglobin [95% CI, 1.07–1.37]) after adjusting for sex, race, ICH severity, time to magnetic resonance imaging, and acute blood pressure change. In secondary analyses, DWI lesions were associated with poor 3-month outcomes (adjusted odds ratio, 1.83 [95% CI, 1.24–2.69]) after adjusting for similar covariates. Conclusions: We identified novel relationships between higher baseline hemoglobin concentrations and DWI ischemic lesions in patients with ICH. Further studies are required to clarify the role of hemoglobin concentration on both cerebral small vessel disease pathophysiology and ICH outcomes.