Monitoring of nighttime EEG slow-wave activity during dexmedetomidine infusion in patients with hyperactive ICU delirium: An observational pilot study.

BACKGROUND: The disturbance of sleep has been associated with intensive care unit (ICU) delirium. Monitoring of EEG slow-wave activity (SWA) has potential in measuring sleep quality and quantity. We investigated the quantitative monitoring of nighttime SWA and its association with the clinical evaluation of sleep in patients with hyperactive ICU delirium treated with dexmedetomidine. METHODS: We performed overnight EEG recordings in 15 patients diagnosed with hyperactive delirium during moderate dexmedetomidine sedation. SWA was evaluated by offline calculation of the C-Trend Index, describing SWA in one parameter ranging 0 to 100 in values. Average and percentage of SWA values <50 were categorized as poor. The sleep quality and depth was clinically evaluated by the bedside nurse using the Richards-Campbell Sleep Questionnaire (RCSQ) with scores <70 categorized as poor. RESULTS: Nighttime SWA revealed individual sleep structures and fundamental variation between patients. SWA was poor in 67%, sleep quality (RCSQ) in 67%, and sleep depth (RCSQ) in 60% of the patients. The category of SWA aligned with that of RCSQ-based sleep quality in 87% and RCSQ-based sleep depth in 67% of the patients. CONCLUSION: Both, SWA and clinical evaluation suggested that the quality and depth of nighttime sleep were poor in most patients with hyperactive delirium despite dexmedetomidine infusion. Furthermore, the SWA and clinical evaluation classifications were not uniformly in agreement. An objective mode such as practical EEG-based solution for sleep evaluation and individual drug dosing in the ICU setting could offer potential in improving sleep for patients with delirium.

Use and outcome of empiric echinocandins in critically ill patients.

BACKGROUND: Echinocandins are recommended as a first-line empiric treatment for fungal infections of patients in an intensive care unit (ICU) with critical illness. The primary aim of the study was to compare outcomes among ICU patients treated with empiric anidulafungin (ANI), caspofungin (CASPO), or micafungin (MICA). METHODS: A retrospective cohort study in a mixed adult ICU. Patient demographics, reason for ICU admission, ICU risk scores and organ support therapies were analyzed. Outcome parameters included ICU and hospital stay, 30-day mortality and 1-year mortality. RESULTS: Empiric echinocandin therapy was given to 367 patients (ANI; 73 patients, CASPO; 84 patients, and MICA; 210 patients) with a median duration of 3 days in an ICU. Patient median age was 60.7 years. As a first-line therapy, 52% of patients received fluconazole. Positive Candida cultures were found in the following samples: blood, 16 (4.4%); central line, 27 (7.4%); deep site, 92 (25.1%). Median ICU stay (ANI 6.4 days, CASPO 5.3 days, MICA 8.1 days), hospital stay (ANI 33 days, CASPO 30 days, MICA 30 days), 30-day mortality (ANI 27%, CASPO 32%, MICA 32%), and 1-year mortality (ANI 33%, CASPO 44%, MICA 45%) did not differ between the groups . The cost of antifungal therapy during the ICU period was similar in the three echinocandin groups (ANI; €1 872, CASPO; €1 799, and MICA; €1783). CONCLUSION: Our results show that ICU, hospital stay, and mortality (hospital, 30-day and 1-year) did not differ among patients with empiric anidulafungin, caspofungin, or micafungin treatment in a mixed adult ICU.

Forehead electrodes sufficiently detect propofol-induced slow waves for the assessment of brain function after cardiac arrest.

In a recent study, we proposed a novel method to evaluate hypoxic ischemic encephalopathy (HIE) by assessing propofol-induced changes in the 19-channel electroencephalogram (EEG). The study suggested that patients with HIE are unable to generate EEG slow waves during propofol anesthesia 48 h after cardiac arrest (CA). Since a low number of electrodes would make the method clinically more practical, we now investigated whether our results received with a full EEG cap could be reproduced using only forehead electrodes. Experimental data from comatose post-CA patients (N = 10) were used. EEG was recorded approximately 48 h after CA using 19-channel EEG cap during a controlled propofol exposure. The slow wave activity was calculated separately for all electrodes and four forehead electrodes (Fp1, Fp2, F7, and F8) by determining the low-frequency (< 1 Hz) power of the EEG. HIE was defined by following the patients' recovery for six months. In patients without HIE (N = 6), propofol substantially increased (244 ± 91%, mean ± SD) the slow wave activity in forehead electrodes, whereas the patients with HIE (N = 4) were unable to produce such activity. The results received with forehead electrodes were similar to those of the full EEG cap. With the experimental pilot study data, the forehead electrodes were as capable as the full EEG cap in capturing the effect of HIE on propofol-induced slow wave activity. The finding offers potential in developing a clinically practical method for the early detection of HIE.

Elevated serum S-100ß in patients with septic shock is associated with delirium.

BACKGROUND: A high prevalence of delirium is observed in sepsis, yet specific markers for this brain dysfunction in sedated patients are still lacking. Cytoplasmic low molecular weight calcium-binding protein, S-100ß, is a commonly used nonspecific marker for brain injury. Here, we evaluated whether delirium is associated with increases in S-100ß levels. METHODS: This observational study included 22 patients with septic shock. Delirium was assessed by CAM-ICU and blood samples were obtained to measure inflammatory (CRP, PCT, IL-6, IL-17, TNF-α) and cerebral biomarkers (S-100ß, NSE, HAB42, SUBP). Patients were categorized according to the presence of delirium. RESULTS: Delirium was present in 10/22 of the patients (45.5%). Serum S-100ß levels were above the laboratory cutoff value of 0.15 µg/L in 13/22 (59.1%) of the patients. The odds ratio for risk of developing delirium in cases with an S-100ß >0.15 µg/L was 18.0 (95%CI, 1.7-196.3, P = 0.011). Patients with delirium had higher plasma levels of IL-6 compared to those without; 138.3 pg/mL [28.0-296.7] vs 53.6 pg/mL [109.3-505, P = 0.050]. There was a positive correlation between S100 ß and IL-6 levels (r = 0.489, P = 0.021). Delirium patients had higher SOFA scores; 10 [5-9] vs 7[8-10.5], P = 0.036. CONCLUSIONS: Delirium in septic shock was associated with an elevated protein S-100ß when using a laboratory cutoff value of 0.15 µg/L and with more severe organ dysfunction during the ICU stay.

Pilot Study of Propofol-induced Slow Waves as a Pharmacologic Test for Brain Dysfunction after Brain Injury.

BACKGROUND: Slow waves (less than 1 Hz) are the most important electroencephalogram signatures of nonrapid eye movement sleep. While considered to have a substantial importance in, for example, providing conditions for single-cell rest and preventing long-term neural damage, a disturbance in this neurophysiologic phenomenon is a potential indicator of brain dysfunction. METHODS: Since, in healthy individuals, slow waves can be induced with anesthetics, the authors tested the possible association between hypoxic brain injury and slow-wave activity in comatose postcardiac arrest patients (n = 10) using controlled propofol exposure. The slow-wave activity was determined by calculating the low-frequency (less than 1 Hz) power of the electroencephalograms recorded approximately 48 h after cardiac arrest. To define the association between the slow waves and the potential brain injury, the patients' neurologic recovery was then followed up for 6 months. RESULTS: In the patients with good neurologic outcome (n = 6), the low-frequency power of electroencephalogram representing the slow-wave activity was found to substantially increase (mean ± SD, 190 ± 83%) due to the administration of propofol. By contrast, the patients with poor neurologic outcome (n = 4) were unable to generate propofol-induced slow waves. CONCLUSIONS: In this experimental pilot study, the comatose postcardiac arrest patients with poor neurologic outcome were unable to generate normal propofol-induced electroencephalographic slow-wave activity 48 h after cardiac arrest. The finding might offer potential for developing a pharmacologic test for prognostication of brain injury by measuring the electroencephalographic response to propofol.

Predictors of hospital and one-year mortality in intensive care patients with refractory status epilepticus: a population-based study.

BACKGROUND: The aim was to determine predictors of hospital and 1-year mortality in patients with intensive care unit (ICU)-treated refractory status epilepticus (RSE) in a population-based study. METHODS: This was a retrospective study of the Finnish Intensive Care Consortium (FICC) database of adult patients (16 years of age or older) with ICU-treated RSE in Finland during a 3-year period (2010-2012). The database consists of admissions to all 20 Finnish hospitals treating RSE in the ICU. All five university hospitals and 11 out of 15 central hospitals participated in the present study. The total adult referral population in the study hospitals was 3.92 million, representing 91% of the adult population of Finland. Patients whose condition had a post-anoxic aetiological basis were excluded. RESULTS: We identified 395 patients with ICU-treated RSE, corresponding to an annual incidence of 3.4/100,000 (95% confidence interval (CI) 3.04-3.71). Hospital mortality was 7.4% (95% CI 0-16.9%), and 1-year mortality was 25.4% (95% CI 21.2-29.8%). Mortality at hospital discharge was associated with severity of organ dysfunction. Mortality at 1 year was associated with older age (adjusted odds ratio (aOR) 1.033, 95% CI 1.104-1.051, p = 0.001), sequential organ failure assessment (SOFA) score (aOR 1.156, CI 1.051-1.271, p = 0.003), super-refractory status epilepticus (SRSE) (aOR 2.215, 95% CI 1.20-3.84, p = 0.010) and dependence in activities of daily living (ADL) (aOR 2.553, 95% CI 1.537-4.243, p < 0.0001). CONCLUSIONS: Despite low hospital mortality, 25% of ICU-treated RSE patients die within a year. Super-refractoriness, dependence in ADL functions, severity of organ dysfunction at ICU admission and older age predict long-term mortality. TRIAL REGISTRATION: Retrospective registry study; no interventions on human participants.

Retinal arterial blood flow and retinal changes in patients with sepsis: preliminary study using fluorescein angiography.

BACKGROUND: Although tissue perfusion is often decreased in patients with sepsis, the relationship between macrohemodynamics and microcirculatory blood flow is poorly understood. We hypothesized that alterations in retinal blood flow visualized by angiography may be related to macrohemodynamics, inflammatory mediators, and retinal microcirculatory changes. METHODS: Retinal fluorescein angiography was performed twice during the first 5 days in the intensive care unit to observe retinal abnormalities in patients with sepsis. Retinal changes were documented by hyperfluorescence angiography; retinal blood flow was measured as retinal arterial filling time (RAFT); and intraocular pressure was determined. In the analyses, we used the RAFT measured from the eye with worse microvascular retinal changes. Blood samples for inflammation and cerebral biomarkers were collected, and macrohemodynamics were monitored. RAFT was categorized as prolonged if it was more than 8.3 seconds. RESULTS: Of 31 patients, 29 (93%) were in septic shock, 30 (97%) required mechanical ventilation, 22 (71%) developed delirium, and 16 (51.6%) had retinal angiopathies, 75% of which were bilateral. Patients with prolonged RAFT had a lower cardiac index before (2.1 L/kg/m2 vs. 3.1 L/kg/m2, P = 0.042) and during angiography (2.1 L/kg/m2 vs. 2.6 L/kg/m2, P = 0.039). They more frequently had retinal changes (81% vs. 20%, P = 0.001) and higher intraocular pressure (18 mmHg vs. 14 mmHg, P = 0.031). Patients with prolonged RAFT had lower C-reactive protein (139 mg/L vs. 254 mg/L, P = 0.011) and interleukin-6 (39 pg/ml vs. 101 pg/ml, P < 0.001) than those with shorter RAFT. CONCLUSIONS: Retinal angiopathic changes were more frequent and cardiac index was lower in patients with prolonged RAFT, whereas patients with shorter filling times had higher levels of inflammatory markers.

Predicting one-year mortality of critically ill patients with early acute kidney injury: data from the prospective multicenter FINNAKI study.

INTRODUCTION: No predictive models for long-term mortality in critically ill patients with acute kidney injury (AKI) exist. We aimed to develop and validate two predictive models for one-year mortality in patients with AKI based on data (1) on intensive care unit (ICU) admission and (2) on the third day (D3) in the ICU. METHODS: This substudy of the FINNAKI study comprised 774 patients with early AKI (diagnosed within 24 hours of ICU admission). We selected predictors a priori based on previous studies, clinical judgment, and differences between one-year survivors and non-survivors in patients with AKI. We validated the models internally with bootstrapping. RESULTS: Of 774 patients, 308 (39.8%, 95% confidence interval (CI) 36.3 to 43.3) died during one year. Predictors of one-year mortality on admission were: advanced age, diminished premorbid functional performance, co-morbidities, emergency admission, and resuscitation or hypotension preceding ICU admission. The area under the receiver operating characteristic curve (AUC) (95% CI) for the admission model was 0.76 (0.72 to 0.79) and the mean bootstrap-adjusted AUC 0.75 (0.74 to 0.75). Advanced age, need for mechanical ventilation on D3, number of co-morbidities, higher modified SAPS II score, the highest bilirubin value by D3, and the lowest base excess value on D3 remained predictors of one-year mortality on D3. The AUC (95% CI) for the D3 model was 0.80 (0.75 to 0.85) and by bootstrapping 0.79 (0.77 to 0.80). CONCLUSIONS: The prognostic performance of the admission data-based model was acceptable, but not good. The D3 model for one-year mortality performed fairly well in patients with early AKI.

Incidence and mortality of super-refractory status epilepticus in adults.

OBJECTIVES: Super-refractory status epilepticus (SRSE) is defined as status epilepticus (SE) that continues or recurs 24h or more after the onset of anesthetic therapy. We defined the incidence and outcome of SRSE in adults in Finland. METHODS: We analyzed retrospectively the Finnish Intensive Care Consortium database in order to identify adult patients with SRSE treated in ICUs in Finland during a three-year period (2010-2012). The database consists of admissions to all 20 Finnish hospitals treating refractory SE (RSE) with general anesthesia in the intensive care unit (ICU). We included consecutive adult (16 years or older) patients with RSE and identified those who had SRSE. Patients with postanoxic etiologies were excluded. RESULTS: All five university hospitals and 10/15 of the central hospitals participated. The adult referral population of the study hospitals is 3.9 million, representing 91% of the total adult population of Finland. We identified 395 patients with ICU-treated RSE, 87 (22%) of whom were classified as having SRSE. This corresponds to an annual incidence of SRSE of 0.7/100,000 (95% confidence interval [CI]: 0.6-0.9). The one-year mortality rates were 36% (95% CI: 26-46%) for patients with SRSE and 22% (95% CI: 17-27%) for patients with RSE. Mortality was highest (63%) in patients with SRSE aged over 75 years. CONCLUSIONS: Approximately 20% of patients with RSE treated in Finnish ICUs progressed to having SRSE. The incidence of SRSE, 0.7/100,000, is about 5-10% of the incidence of SE. The mortality of patients with SRSE, 36%, was comparable to earlier studies and twofold higher than the mortality of patients with RSE. This article is part of a Special Issue entitled "Status Epilepticus".

Variation in the use of renal replacement therapy in patients with septic shock: a substudy of the prospective multicenter observational FINNAKI study.

INTRODUCTION: Indications for renal replacement therapy (RRT) have not been generally standardized and vary among intensive care units (ICUs). We aimed to assess the proportion, indications, and modality of RRT, as well as the association between the proportion of RRT use and 90-day mortality in patients with septic shock in Finnish adult ICUs. METHODS: We identified patients with septic shock from the prospective observational multicenter FINNAKI study conducted between 1 September 2011 and 1 February 2012. We divided the ICUs into high-RRT and low-RRT ICUs according to the median of the proportion of RRT-treated patients with septic shock. Differences in indications, and modality of RRT between ICU groups were assessed. Finally, we performed an adjusted logistic regression analysis to evaluate the possible association of the ICU group (high vs. low-RRT) with 90-day mortality. RESULTS: Of the 726 patients with septic shock, 131 (18.0%, 95% CI 15.2 to 20.9%) were treated with RRT. The proportion of RRT-treated patients varied from 3% up to 36% (median 19%) among ICUs. High-RRT ICUs included nine ICUs (354 patients) and low-RRT ICUs eight ICUs (372 patients). In the high-RRT ICUs patients with septic shock were older (P = 0.04), had more cardiovascular (P <0.001) and renal failures (P = 0.003) on the first day in the ICU, were more often mechanically ventilated, and received higher maximum doses of norepinephrine (0.25 µg/kg/min vs. 0.18 µg/kg/min, P <0.001) than in the low-RRT ICUs. No significant differences in indications for or modality of RRT existed between the ICU groups. The crude 90-day mortality rate for patients with septic shock was 36.2% (95% CI 31.1 to 41.3%) in the high-RRT ICUs compared to 33.9% (95% CI 29.0 to 38.8%) in the low-RRT ICUs, P = 0.5. In an adjusted logistic regression analysis the ICU group (high-RRT or low-RRT ICUs) was not associated with 90-day mortality. CONCLUSIONS: Patients with septic shock in ICUs with a high proportion of RRT had more severe organ dysfunctions and received more organ-supportive treatments. Importantly, the ICU group (high-RRT or low-RRT group) was not associated with 90-day mortality.

Age of red blood cells and outcome in acute kidney injury.

INTRODUCTION: Transfusion of red blood cells (RBCs) and, in particular, older RBCs has been associated with increased short-term mortality in critically ill patients. We evaluated the association between age of transfused RBCs and acute kidney injury (AKI), hospital, and 90-day mortality in critically ill patients. METHODS: We conducted a prospective, observational, predefined sub-study within the FINNish Acute Kidney Injury (FINNAKI) study. This study included all elective ICU admissions with expected ICU stay of more than 24 hours and all emergency admissions from September to November 2011. To study the age of RBCs, we classified transfused patients into quartiles according to the age of oldest transfused RBC unit in the ICU. AKI was defined according to KDIGO (Kidney Disease: Improving Global Outcomes) criteria. RESULTS: Out of 1798 patients, 652 received at least one RBC unit. The median [interquartile range] age of the oldest RBC unit transfused was 12 [11-13] days in the freshest quartile and 21 [17-27] days in the quartiles 2 to 4. On logistic regression, RBC age was not associated with the development of KDIGO stage 3 AKI. Patients in the quartile of freshest RBCs had lower crude hospital and 90-day mortality rates compared to those in the quartiles of older blood. After adjustments, older RBC age was associated with significantly increased risk for hospital mortality. Age, Simplified Acute Physiology Score II (SAPS II)-score without age points, maximum Sequental Organ Failure Assessment (SOFA) score and the total number of transfused RBC units were independently associated with 90-day mortality. CONCLUSIONS: The age of transfused RBC units was independently associated with hospital mortality but not with 90-day mortality or KDIGO stage 3 AKI. The number of transfused RBC units was an independent risk factor for 90-day mortality.

Repolarization abnormalities in patients with subarachnoid and intracerebral hemorrhage: predisposing factors and association with outcome.

BACKGROUND: Electrocardiographic (ECG) abnormalities are frequent in patients with intracranial insult. In this study, we evaluated the factors predisposing to the repolarization abnormalities, i.e., prolonged corrected QT (QTc) interval, ischemic-like ECG changes and morphologic end-repolarization abnormalities, and examined the prognostic value of these abnormalities in patients with subarachnoid and intracerebral hemorrhages requiring intensive care. METHODS: This was a prospective, observational clinical study in a university-level intensive care unit. Clinical characteristics, the level of consciousness, and findings in primary head computed tomography were recorded on admission. The study period was divided into three 2-day sections. In each section, a 12-lead ECG, transthoracic echocardiography, the results of standard blood electrolytes and cardiac troponin I, as well as the rate of vasoactive and sedative drug infusions were recorded. Repolarization abnormalities such as prolongation of the QTc interval (millisecond), ischemic-like ECG changes, and morphologic end-repolarization abnormalities (present/absent) were evaluated and analyzed. The 1-year functional outcome was determined using the Glasgow Outcome Score. RESULTS: During the 2-year study period, 108 patients were included in the study. Different repolarization abnormalities were frequent in both types of hemorrhage. Prolongation of the QTc interval was predisposed by female gender (ß, 24.5; P = 0.010) and the use of propofol (ß, 30.5; P = 0.001). The predisposing factor for ischemic-like ECG changes were male gender (odds ratio [OR], 5.9; P = 0.003) and for morphological end-repolarization abnormalities aneurysmatic bleeding (OR, 13.0; P = 0.002). Ischemic-like ECG changes were common, in 87/108 patients during the study period, and were associated with a poorer 1-year functional outcome (OR, 4.7; lower 95% confidence interval, 1.5; P = 0.010). CONCLUSIONS: Each repolarization abnormality has characteristic predisposing factors. Ischemic-like ECG changes are common and are associated with a poorer 1-year functional outcome.

Neurogenic pulmonary edema in patients with nontraumatic intracerebral hemorrhage: predictors and association with outcome.

BACKGROUND: Neurogenic pulmonary edema (NPE) is a well-recognized phenomenon after intracranial insult. In this study, we evaluated the predictors for NPE and its association with outcome in patients with intensive care unit-treated nontraumatic intracranial hemorrhage. METHODS: This was a prospective, observational clinical study in a university-level intensive care unit. Clinical characteristics, level of consciousness, and Acute Physiology and Chronic Health Evaluation (APACHE) II score were recorded on admission and the findings of primary head computed tomography were reviewed. A chest radiograph and arterial blood gas analysis were taken serially and NPE was determined as acute bilateral infiltrates in chest radiograph and hypoxemia. Echocardiography and cardiac and inflammatory markers were recorded. The 1-year outcome was assessed using the Glasgow Outcome Scale. RESULTS: NPE developed in 38 (35%) of the 108 patients included. Predictors for NPE were higher APACHE II score (≥20, odds ratio 6.17, P = 0.003) and higher interleukin-6 plasma concentration (>40 pg/mL, odds ratio 5.62, P = 0.003). Of patients with 0, 1, or 2 predictors mentioned above, 4%, 37%, and 65% had NPE, respectively. NPE was associated with a higher 1-year mortality (37% vs 14%, P = 0.007, respectively), but with an unchanged functional outcome after 1 year (Glasgow Outcome Scale score 1-3, 53% vs 51%, P > 0.9). CONCLUSIONS: Predictors for NPE are the severity of disease defined by APACHE II scores and higher levels of systemic inflammatory mediators. NPE is associated with a higher 1-year mortality, but not with a poorer 1-year functional outcome.

Effect of acute pancreatitis on porcine intestine: a morphological study.

AIM: The ultrastructural changes in the intestine were studied during experimental acute edematous and necrotizing porcine pancreatitis. The immunohistochemical expression of E-cadherin and ß-catenin in the jejunum and colon was assessed to characterize changes in the adherens junctions. METHODS: Twenty-four pigs were randomized to controls (n = 8) or to develop mild edematous (n = 8, saline infusion to pancreatic duct) or severe necrotizing pancreatitis (n = 8, taurocholic acid infusion). The ultrastructure of the mesenteric artery and the vein and epithelium of the jejunum and colon was analyzed at baseline and after 540 min with electron microscopy. The expression of E-cadherin and ß-catenin was assessed with immunohistochemistry. RESULTS: In the colon the microvilli and their glycocalyx shortened and reduced in density the most in necrotizing pancreatitis. In necrotizing pancreatitis adherens and tight junctions were occasionally open in the colon but rarely in the jejunum. Mitochondria in the colon epithelial cells were degenerated in necrotizing pancreatitis, swollen in edematous pancreatitis, and remained intact in the control case. In necrotizing pancreatitis, capillaries of the colon showed a broken endothelial lining with narrow lumens. The expression of E-cadherin immunoreactivity showed a trend toward a decrease in the colon in both edematous and necrotizing pancreatitis. CONCLUSION: Ultrastructural abnormalities in acute pancreatitis appear early in the colon, where they seem to be more damaging than in jejunum. Epithelial cell damage seems to include mitochondrial injury and an opening of tight and adherens junctions, which are more pronounced in necrotizing pancreatitis. Damage is seen in the mucosal and mesenteric endothelial cells.

Portal vein cytokines in the early phase of acute experimental oedematous and necrotizing porcine pancreatitis.

OBJECTIVE: Cytokines initiate and modify systemic inflammatory response in early acute pancreatitis. The aim of this study was to analyze which cytokines are released from the pancreas to portal venous blood in the early phase of acute experimental necrotizing and oedematous pancreatitis and which of those cytokines are correlated with the more severe form of the disease. MATERIAL AND METHODS: Fifteen pigs were randomized to develop mild oedematous pancreatitis (n = 5, saline infusion to pancreatic duct), severe necrotizing pancreatitis (n = 5, taurocholic acid infusion) along with a control group (n = 5). Arterial and venous blood samples were drawn and cytokine levels were measured from portal vein blood at 0, 120, 240 and 360 min after the induction of pancreatitis. Tissue samples from the pancreas were harvested at 0 and 360 min. RESULTS: White blood cell count increased in necrotizing pancreatitis and the control group. The amount of neutrophils increased (p < 0.001) and the lymphocyte and eosinophil counts decreased in all groups (p < 0.001, p < 0.001). The monocyte count, as well as PDGF and IL-6 concentrations, increased only in necrotizing pancreatitis. IL-8 and eotaxin increased both in oedematous and necrotizing pancreatitis. MCP-1 increased in all groups. IL-9, IL-4, MIP-1α, IFN- γ concentrations did not change. Eotaxin and MCP-1 plasma levels from a previous series between portal venous and pulmonary arterial blood were not significantly different. CONCLUSIONS: The initial inflammatory process was diverse in oedematous and necrotizing pancreatitis. Increased monocyte count in combination with elevated PDGF and IL-6 are characteristic of necrotizing pancreatitis in our model.

Intestinal bacterial translocation and tight junction structure in acute porcine pancreatitis.

BACKGROUND/AIMS: To examine whether intestinal bacterial translocation occurs early in acute mild and severe pancreatitis and whether the intestinal expression of tight junction proteins (claudins-2, -3, -4, -5, -7), apoptosis or proliferation would explain the possible translocation. METHODOLOGY: Fifteen pigs were randomized to controls (n=5) or to develop mild edematous pancreatitis (n=5, saline infusion to pancreatic duct) or severe necrotic pancreatitis (n=5, taurocholic acid infusion). Translocation was studied by measuring bacterial cultures from portal vein blood and mesenteric lymph nodes. Immunohistochemical expression of the tight junction proteins, apoptosis rate (TUNEL) and Ki-67 were analyzed quantitatively from the epithelium of the jejunum and colon. RESULTS: There was no bacterial translocation during the 6 hours followup, nor changes in the expression of tight junction proteins claudins-2 and -5 in jejunum or colon. Saturation and proportional area of claudin-3 staining decreased in the colon, as did claudins-4 and -7 staining in the jejunum of the necrotic pancreatitis group. Increased apoptosis was found in all samples from controls and the edematous pancreatitis group but not in jejunum in the necrotic pancreatitis group. Ki-67 activity tended to increase in the upper half of the villus in edematous and necrotic pancreatitis. There were no changes in the basic histology. CONCLUSIONS: The major finding of this study was that bacterial translocation from the gut is not present at the beginning of acute pancreatitis. Tight junction proteins claudin-2 and -5 do not become altered in the early stages of pancreatitis. Claudin-3 decreases in the colon and claudins-4 and -7 in the jejunum in necrotic pancreatitis. Laparotomy itself causes increased apoptosis in the colon and the jejunum.

Early recovery of frontal EEG slow wave activity during propofol sedation predicts outcome after cardiac arrest.

AIM OF THE STUDY: EEG slow wave activity (SWA) has shown prognostic potential in post-resuscitation care. In this prospective study, we investigated the accuracy of continuously measured early SWA for prediction of the outcome in comatose cardiac arrest (CA) survivors. METHODS: We recorded EEG with a disposable self-adhesive frontal electrode and wireless device continuously starting from ICU admission until 48 h from return of spontaneous circulation (ROSC) in comatose CA survivors sedated with propofol. We determined SWA by offline calculation of C-Trend® Index describing SWA as a score ranging from 0 to 100. The functional outcome was defined based on Cerebral Performance Category (CPC) at 6 months after the CA to either good (CPC 1-2) or poor (CPC 3-5). RESULTS: Outcome at six months was good in 67 of the 93 patients. During the first 12 h after ROSC, the median C-Trend Index value was 38.8 (interquartile range 28.0-56.1) in patients with good outcome and 6.49 (3.01-18.2) in those with poor outcome showing significant difference (p < 0.001) at every hour between the groups. The index values of the first 12 h predicted poor outcome with an area under curve of 0.86 (95% CI 0.61-0.99). With a cutoff value of 20, the sensitivity was 83.3% (69.6%-92.3%) and specificity 94.7% (83.4%-99.7%) for categorization of outcome. CONCLUSION: EEG SWA measured with C-Trend Index during propofol sedation offers a promising practical approach for early bedside evaluation of recovery of brain function and prediction of outcome after CA.

Automatic detection of artifacts in EEG by combining deep learning and histogram contour processing.

This paper introduces a simple approach combining deep learning and histogram contour processing for automatic detection of various types of artifact contaminating the raw electroencephalogram (EEG). The proposed method considers both spatial and temporal information of raw EEG, without additional need for reference signals like ECG or EOG. The proposed method was evaluated with data including 785 EEG sequences contaminated by artifacts and 785 artifact-free EEG sequences collected from 15 intensive care patients. The obtained results showed an overall accuracy of 0.98, representing high reliability of proposed technique in detecting different types of artifacts and being comparable or outperforming the approaches proposed earlier in the literature.

A Correlation-Driven Mapping For Deep Learning application in detecting artifacts within the EEG.

OBJECTIVE: When developing approaches for automatic preprocessing of electroencephalogram (EEG) signals in non-isolated demanding environment such as intensive care unit (ICU) or even outdoor environment, one of the major concerns is varying nature of characteristics of different artifacts in time, frequency and spatial domains, which in turn causes a simple approach to be not enough for reliable artifact removal. Considering this, current study aims to use correlation-driven mapping to improve artifact detection performance. APPROACH: A framework is proposed here for mapping signals from multichannel space (regardless of the number of EEG channels) into two-dimensional RGB space, in which the correlation of all EEG channels is simultaneously taken into account, and a deep convolutional neural network (CNN) model can then learn specific patterns in generated 2D representation related to specific artifact. MAIN RESULTS: The method with a classification accuracy of 92.30% (AUC = 0.96) in a leave-three-subjects-out cross-validation procedure was evaluated using data including 2310 EEG sequences contaminated by artifacts and 2285 artifact-free EEG sequences collected with BrainStatus self-adhesive electrode and wireless amplifier from 15 intensive care patients. For further assessment, several scenarios were also tested including performance variation of proposed method under different segment lengths, different numbers of isoline and different numbers of channel. The results showed outperformance of CNN fed by correlation coefficients data over both spectrogram-based CNN and EEGNet on the same dataset. SIGNIFICANCE: This study showed the feasibility of utilizing correlation image of EEG channels coupled with deep learning as a promising tool for dimensionality reduction, channels fusion and capturing various artifacts patterns in temporal-spatial domains. A simplified version of proposed approach was also shown to be feasible in real-time application with latency of 0.0181 s for making real-time decision.

Leukocyte filter enhances neutrophil activation during combined aortic valve and coronary artery bypass surgery.

OBJECTIVE: Cardiopulmonary bypass-induced systemic inflammatory reaction involving the expression of neutrophil surface adhesion molecules is the main mechanism leading to myocardial ischemia-reperfusion injury as well as multiorgan dysfunction. Patients undergoing prolonged cardiopulmonary bypass are especially at risk in this regard. The aim of this prospective, randomized study was to evaluate the impact of continuous leukocyte filtration on the perioperative expression of neutrophil adhesion molecules along with the markers of systemic inflammation during combined coronary artery revascularization and aortic valve surgery due to aortic stenosis. PATIENT AND METHODS: Twenty patients scheduled for combined coronary artery revascularization and aortic valve surgery due to aortic stenosis were randomized to undergo cardiopulmonary bypass with or without a leukocyte filter (LeukoGuard LG6). The expression of neutrophil adhesion molecules and proinflammatory cytokine response were measured. RESULTS: The use of the leukocyte filter significantly increased neutrophil CD11b expression (Pg = .003) compared to the control group, which was followed by a faster rise in interleukin-6 levels 5 minutes (median, 125 versus 34 pg/mL) and 2 hours after cardiopulmonary bypass (median, 158 versus 92 pg/mL, Pt x g < .001), respectively. No marked differences in terms of levels of CD11a, CD62L, cardiac troponin-I, or oxyhemodynamics were observed. CONCLUSIONS: The observed increased neutrophil activation and enhanced inflammatory response do not support the use of continuous leukofiltration in patients undergoing prolonged cardiopulmonary bypass.