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Objective: To investigate the effects of the combination of extracorporeal cardiopulmonary resuscitation and thrombolytic therapy on the recovery of vital organ function after prolonged cardiac arrest. Design: Laboratory investigation. Setting: University laboratory. Subjects: Pigs. Interventions: Animals underwent 30-minute untreated ventricular fibrillation cardiac arrest followed by extracorporeal cardiopulmonary resuscitation for 6 hours. Animals were allocated into two experimental groups: t-extracorporeal cardiopulmonary resuscitation (t-ECPR) group, which received streptokinase 1 million units, and control extracorporeal cardiopulmonary resuscitation (c-ECPR), which did not receive streptokinase. In both groups, the resuscitation protocol included the following physiologic targets: mean arterial pressure greater than 70 mm Hg, cerebral perfusion pressure greater than 50 mm Hg, PaO2 150 ± 50 torr (20 ± 7 kPa), Paco2 40 ± 5 torr (5 ± 1 kPa), and core temperature 33°C ± 1°C. Defibrillation was attempted after 30 minutes of extracorporeal cardiopulmonary resuscitation. Measurements and Main Results: A cardiac resuscitability score was assessed on the basis of success of defibrillation, return of spontaneous heart beat, weanability from extracorporeal cardiopulmonary resuscitation, and left ventricular systolic function after weaning. The addition of thrombolytic to extracorporeal cardiopulmonary resuscitation significantly improved cardiac resuscitability (3.7 ± 1.6 in t-ECPR vs 1.0 ± 1.5 in c-ECPR). Arterial lactate clearance was higher in t-ECPR than in c-ECPR (40% ± 15% vs 18% ± 21%). At the end of the experiment, the intracranial pressure was significantly higher in c-ECPR than in t-ECPR. Recovery of brain electrical activity, as assessed by quantitative analysis of electroencephalogram signal, and ischemic neuronal injury on histopathologic examination did not differ between groups. Animals in t-ECPR group did not have increased bleeding complications, including intracerebral hemorrhages. Conclusions: In a porcine model of prolonged cardiac arrest, t-ECPR improved cardiac resuscitability and reduced brain edema, without increasing bleeding complications. However, early electroencephalogram recovery and ischemic neuronal injury were not improved.

Objectives: The gamma-aminobutyric acid modulator propofol induces neuronal cell death in healthy immature brains by unbalancing neurotrophin homeostasis via p75 neurotrophin receptor signaling. In adulthood, p75 neurotrophin receptor becomes down-regulated and propofol loses its neurotoxic effect. However, acute brain lesions, such as traumatic brain injury, reactivate developmental-like programs and increase p75 neurotrophin receptor expression, probably to foster reparative processes, which in turn could render the brain sensitive to propofol-mediated neurotoxicity. This study investigates the influence of delayed single-bolus propofol applications at the peak of p75 neurotrophin receptor expression after experimental traumatic brain injury in adult mice. Design: Randomized laboratory animal study. Setting: University research laboratory. Subjects: Adult C57BL/6N and nerve growth factor receptor–deficient mice. Interventions: Sedation by IV propofol bolus application delayed after controlled cortical impact injury. Measurements and Main Results: Propofol sedation at 24 hours after traumatic brain injury increased lesion volume, enhanced calpain-induced ?II-spectrin cleavage, and increased cell death in perilesional tissue. Thirty-day postinjury motor function determined by CatWalk (Noldus Information Technology, Wageningen, The Netherlands) gait analysis was significantly impaired in propofol-sedated animals. Propofol enhanced pro–brain-derived neurotrophic factor/brain-derived neurotrophic factor ratio, which aggravates p75 neurotrophin receptor–mediated cell death. Propofol toxicity was abolished both by pharmacologic inhibition of the cell death domain of the p75 neurotrophin receptor (TAT-Pep5) and in mice lacking the extracellular neurotrophin binding site of p75 neurotrophin receptor. Conclusions: This study provides first evidence that propofol sedation after acute brain lesions can have a deleterious impact and implicates a role for the pro–brain-derived neurotrophic factor-p75 neurotrophin receptor pathway. This observation is important as sedation with propofol and other compounds with GABA receptor activity are frequently used in patients with acute brain pathologies to facilitate sedation or surgical and interventional procedures.

Objectives: The availability of a fast and reliable sodium result is a prerequisite for the appropriate correction of a patient’s fluid balance. Blood gas analyzers and core laboratory chemistry analyzers measure electrolytes via different ion-selective electrode methodology, that is, direct and indirect ion-selective electrodes, respectively. Sodium concentrations obtained via both methods are not always concordant. A comparison of results between both methods was performed, and the impact of the total protein concentration on the sodium concentration was investigated. Furthermore, we sought to develop an adjustment equation to correct between both ion-selective electrode methods. Design: A model was developed using a pilot study cohort (n = 290) and a retrospective patient cohort (n = 690), which was validated using a prospective patient cohort (4,006 samples). Setting: ICU and emergency department at Ghent University Hospital. Patients: Patient selection was based on the concurrent availability of routine blood gas Na+direct as well as core laboratory Na+indirect results. Interventions: In the pilot study, left-over blood gas syringes were collected for further laboratory analysis. Measurement and Main Results: There was a significant negative linear correlation between Na+indirect and Na+direct relative to changes in total protein concentration (Pearson r = –0.69; p < 0.0001). In our setting, for each change of 10 g/L in total protein concentration, a deviation of ~1.3 mmol/L is observed with the Na+indirect result. Validity of our adjustment equation protein-corrected Na+indirect = Na+indirect – 10.53 + (0.1316 × total protein) was demonstrated on a prospective patient cohort. Conclusions: As Na+direct measurements on a blood gas analyzer are not influenced by the total protein concentration in the sample, they should be preferentially used in patients with abnormal protein concentrations. However, as blood gas analyzers are not available at all clinical wards, the implementation of a protein-corrected sodium result might provide an acceptable alternative.

Objectives: To test the hypothesis that nebulized epinephrine ameliorates pulmonary dysfunction by dual action—bronchodilation (?2-adrenergic receptor agonism) and attenuation of airway hyperemia (?1-adrenergic receptor agonism) with minimal systemic effects. Design: Randomized, controlled, prospective, and large animal translational studies. Setting: University large animal ICU. Subjects: Twelve chronically instrumented sheep. Interventions: The animals were exposed to 40% total body surface area third degree skin flame burn and 48 breaths of cooled cotton smoke inhalation under deep anesthesia and analgesia. The animals were then placed on a mechanical ventilator, fluid resuscitated, and monitored for 48 hours in a conscious state. After the injury, sheep were randomized into two groups: 1) epinephrine, nebulized with 4 mg of epinephrine every 4 hours starting 1 hour post injury, n = 6; or 2) saline, nebulized with saline in the same manner, n = 6. Measurements and Main Results: Treatment with epinephrine had a significant reduction of the pulmonary transvascular fluid flux to water (p < 0.001) and protein (p < 0.05) when compared with saline treatment from 12 to 48 hours and 36 to 48 hours, respectively. Treatment with epinephrine also reduced the systemic accumulation of body fluids (p < 0.001) with a mean of 1,410 ± 560 mL at 48 hours compared with 3,284 ± 422 mL of the saline group. Hemoglobin levels were comparable between the groups. Changes in respiratory system dynamic compliance, mean airway pressure, PaO2/FiO2 ratio, and oxygenation index were also attenuated with epinephrine treatment. No considerable systemic effects were observed with epinephrine treatment. Conclusions: Nebulized epinephrine should be considered for use in future clinical studies of patients with burns and smoke inhalation injury.

Objective: This special article will review the history of blood glucose meter hospital use and current issues surrounding their use in this patient population. Study Selection: Secondary to accuracy concerns that have been known, but likely underappreciated for many years, the U.S. Food and Drug Administration and Centers for Medicare and Medicaid Services are moving toward eliminating current blood glucose meters for use with critically ill patients. Data Sources: Recent guidance from the U.S. Food and Drug Administration and Centers for Medicare and Medicaid Services along with several recent publications will be used as the primary data sources. Data Extraction: U.S. Food and Drug Administration, Centers for Medicare and Medicaid Services communications combined with recent interpretation of this guidance were used to provide this overview. Data Synthesis: Centers for Medicare and Medicaid Services have issued a temporary moratorium on the prohibition of the use of blood glucose meters in the critically ill. They have not given a deadline for the moratorium or solicited comments. Conclusions: Physicians who care for critically ill patients need to be cognizant of the accuracy and interference limitations of blood glucose meters and aware of the current regulatory situation.

Objective: To report a series of three patients who received simultaneous circulatory support with both veno-arterial extracorporeal membrane oxygenation and intra-aortic balloon pump and subsequently developed spinal cord infarction, and present a brief review of the relevant literature. Data Sources: Hospital medical records and MEDLINE and PubMed databases. Study Selection: Any patient who developed lower limb neurologic symptoms during a period of concurrent venoarterial extracorporeal membrane oxygenation and intra-aortic balloon pump support, with subsequent MRI changes involving the spinal cord, from 2006 (the year of institution of venoarterial extracorporeal membrane oxygenation in our ICU) to 2014. Data Extraction: Patient records were retrospectively reviewed. Medical databases were searched for any literature linking intra-aortic balloon pump and/or venoarterial extracorporeal membrane oxygenation with neurologic injury of the lower limbs. Data Synthesis: Three female patients presented in cardiogenic shock or arrest requiring circulatory support. Intra-aortic balloon pump was inserted, and peripheral veno-arterial extracorporeal membrane oxygenation was initiated with subsequent loss of native ejection in each case. Neurologic signs were noted clinically, and subsequent imaging demonstrated spinal cord infarction and small aortic size for all three patients. Conclusions: The timeline of events suggests a causal relation between intra-aortic balloon pump, veno-arterial extracorporeal membrane oxygenation, and significant neurologic deficits. This is likely due to hypoperfusion of the spinal cord, which is multifactorial in origin, including small aortic calibre, low cardiac output states, high vasopressor requirements causing vasospasm of the artery of Adamkiewicz, occlusion of retrograde oxygenated blood flow from peripheral veno-arterial extracorporeal membrane oxygenation due to intra-aortic balloon pump being in situ, and possible thromboembolic phenomena. The thoracic spinal cord is intrinsically susceptible to ischemia due to the anatomy of the arterial supply, which is described here. We identify several risk factors and make several recommendations to avoid this rare but catastrophic complication in the future. We also suggest interventions should this challenging complication be identified.

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