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Eighteen Pediococcus strains were screened for their potential as silage inoculants. Pediococcus acidilactici G24 was found to be the most suitable, exhibiting a short lag phase on both glucose and fructose, a rapid rate of acid production, a high sugar-to-lactate conversion efficiency, no detectable breakdown of proteins or lactic acid, and the ability to grow within a broad range of pH and temperature. When tested in laboratory silos using grass with a water-soluble carbohydrate content of 24 gfkg of aqueous extract, P. acidilactici G24 stimulated the natural LactobaciUus plantarum population and accelerated the rates of lactic acid production and pH decrease. After 6 days of fermentation, the inoculated silage exhibited a 12% decrease in ammonia nitrogen and an 11% increase in crude protein levels compared with uninoculated controls. The use of an L. plantarum inoculant at a rate of 104 bacteria per g of grass in conjunction with P. acidilactici G24 produced no additional beneficial effect. Inoculation of grass with a water-soluble carbohydrate level of 8 g/kg of aqueous extract with P. acidilactici G24 led to no acceleration in the rate of L. plantarum growth or pH decrease. However, after 7 days of fermentation the inoculated silage had a 14% lower ammonia nitrogen protein content than did uninoculated controls. The results suggest that P. acidilactici G24 may be useful as a silage inoculant for crops with a sufficiently high water-soluble carbohydrate level.

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In 2000, the Society of Critical Care Medicine (SCCM) and the American College of Clinical Pharmacy (ACCP) published a position paper that defined critical care pharmacy services as fundamental, desirable, and optimal. A task force was developed that included individuals who are members of the ACCP Critical Care Practice and Research Network, the SCCM clinical pharmacy and pharmacology section, and the American Society of Health‐System Pharmacists to develop an opinion paper with three primary objectives: to provide recommendations for the level of preparation and training of pharmacists to practice in critical care, to develop recommendations for the credentialing of pharmacists providing critical care services, and to develop mechanisms for documenting and justifying intensive care unit (ICU) pharmacy services. Each objective was addressed to accommodate the levels of services defined as fundamental, desirable, or optimal, and are targeted at all pharmacists providing or wanting to provide pharmacy services to critically ill patients. The training and preparing of the pharmacist caring for critically ill patients is discussed in the context of the knowledge and skills required to provide pharmacy services in the ICU. Credentialing of the critical care pharmacist and the documentation of services take into account the various scopes of practice, and recommendations are based on current and idealistic mechanisms. A detailed outline is provided for the process of services justification. This paper provides a foundation that is focused on delivering direct and proactive patient care services, particularly at the desirable and optimal levels, with the ultimate goal of enhancing the level of pharmacy services provided to the care of critically ill patients. This commentary should be of interest to numerous stakeholders including pharmacists, other pharmacy department staff, other ICU health care professionals, hospital and academic administrators, accrediting agencies, government officials, and payers. The task force encourages the profession of pharmacy in general to incorporate key recommendations provided in this document with respect to specialized training, credentialing, and service justification.

Introduction Anticoagulation, fibrinogen consumption, fibrinolytic activation, and platelet dysfunction all interact to produce different clot formation responses after trauma. However, the relative contributions of these coagulation components to overall clot formation remains poorly defined. We examined for sources of heterogeneity in clot formation responses after trauma. Methods Blood was sampled in the Emergency Department from patients meeting trauma team activation criteria at an urban trauma center. Plasma prothrombin time (PT) ≥ 18 sec was used to define traumatic coagulopathy. Mean kaolin-activated thrombelastography (TEG) parameters were calculated and tested for heterogeneity using Analysis of Means (ANOM). Discriminant analysis and forward stepwise variable selection with linear regression were used to determine if PT, fibrinogen, platelet contractile force (PCF), and D-Dimer concentration, representing key mechanistic components of coagulopathy, each contribute to heterogeneous TEG responses after trauma. Results Of 95 subjects, 16% met criteria for coagulopathy. Coagulopathic subjects were more severely injured with greater shock, and received more blood products in the first 8 hours compared to non-coagulopathic subjects. Mean (SD) TEG maximal amplitude (MA) was significantly decreased in the coagulopathic group=57.5 (4.7) mm, vs. 62.7 (4.7), T test p<0.001. The MA also exceeded the ANOM predicted upper decision limit for the non-coagulopathic group and the lower decision limit for the coagulopathic group at alpha=0.05, suggesting significant heterogeneity from the overall cohort mean. Fibrinogen and PCF best discriminated TEG MA using discriminant analysis. Fibrinogen, PCF, and D-Dimer were primary covariates for TEG MA using regression analysis. Conclusion Heterogeneity in TEG-based clot formation in Emergency Department trauma patients was linked to changes in MA. Individual parameters representing fibrin polymerization, platelet contractile forces, and fibrinolysis were primarily associated with TEG MA after trauma and should be the focus of early hemostatic therapies.

Platelets in trauma‐induced coagulopathy (TIC) are impaired, but the mechanism is not known. We performed comprehensive longitudinal platelet function testing in trauma patient samples. Platelets in TIC are widely impaired early after injury, but platelet activatability is intact. This suggests a mechanism of transient platelet cytoskeletal/integrin dysfunction during TIC. Summary BackgroundTrauma‐induced coagulopathy (TIC) is a common and deadly bleeding disorder. Platelet dysfunction is present during TIC, but its mechanisms remain unclear. Platelets are currently thought to become “exhausted,” a state in which they have released their granule contents and can no longer aggregate or contract. MethodsThis prospective observational cohort study tested the hypothesis that platelet exhaustion is present during TIC and characterized the early time course of platelet dysfunction. Blood was collected from 95 adult trauma patients at a Level I trauma center at time of Emergency Department arrival and several time points over 72 h. Platelet activation state and function were characterized using CD62P (P‐selectin) and PAC‐1 surface membrane staining, platelet function analyzer (PFA‐100), aggregometry, viscoelastic platelet mapping, and, to test for exhaustion, their ability to express CD62P after ex vivo adenosine diphosphate (ADP) agonism. Platelet function was compared between patients with and without TIC, defined by prothrombin time ≥18 s. ResultsPlatelets in TIC showed no initial increase in their level of surface activation markers or impairment of their capacity to express CD62P in response to ADP stimulation. However, TIC platelets were impaired in nearly all functional assays, spanning adhesion, aggregation, and contraction. These effects largely remained after controlling for platelet count and fibrinogen concentration and resolved after 8 h. ConclusionThe TIC platelets exhibit early impairment of adhesion, aggregation, and contraction with retained alpha granule secretion ability, suggesting a specific mechanism of cytoskeletal or integrin dysfunction that is not a result of more general platelet exhaustion.

Background Trauma-induced coagulopathy is a complex multifactorial hemostatic response that is poorly understood. Objectives Identify distinct hemostatic responses to trauma and identify key components of the hemostatic system that vary between responses. Patients/Methods Cross-sectional observational study of adult trauma patients at an urban Level I trauma center Emergency Department. Hierarchical clustering analysis was used to identify distinct clusters of similar subjects using vital signs, injury/shock severity, and by comprehensive assessment of coagulation, clot formation, platelet function, and thrombin generation. Results Of 84 total trauma patients included in the model, three distinct trauma clusters were identified. Cluster 1 (N=57) displayed platelet activation, preserved peak thrombin generation, plasma coagulation dysfunction, moderately decreased fibrinogen concentration, and normal clot formation relative to healthy controls. Cluster 2 (N=18) displayed platelet activation, preserved peak thrombin generation, and preserved fibrinogen concentration with normal clot formation. Cluster 3 (N=9) was the most severely injured and shocked and displayed a strong inflammatory and bleeding phenotype. Platelet dysfunction, thrombin inhibition, plasma coagulation dysfunction, and decreased fibrinogen concentration were present in this cluster. Fibrinolytic activation was present in all clusters, but increased more so in Cluster 3. Trauma clusters were different most noticeably in their relative fibrinogen concentration, peak thrombin generation, and platelet-induced clot contraction. Conclusions Hierarchical clustering analysis identified 3 distinct hemostatic responses to trauma. Further insight into the underlying hemostatic mechanisms responsible for these responses is needed.

The diagnosis and management of seizures in the critically ill patient can sometimes present a unique challenge for practitioners due to lack of exposure and complex patient comorbidities. The reported incidence varies between 8% and 34% of critically ill patients, with many patients often showing no overt clinical signs of seizures. Outcomes in patients with unidentified seizure activity tend to be poor, and mortality significantly increases in those who have seizure activity longer than 30 min. Prompt diagnosis and provision of medical therapy are crucial in order to attain successful seizure termination and prevent poor outcomes. In this article, we review the epidemiology and pathophysiology of seizures in the critically ill, various seizure monitoring modalities, and recommended medical therapy.