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Spyros Zakynthinos

Publications and source records attributed to Spyros Zakynthinos.

18 recordsLinked to original sources
PubMed2007

Angiopoietin-2 is increased in severe sepsis: correlation with inflammatory mediators.

OBJECTIVE: Angiopoietin (Ang)-2 is an endothelium-specific growth factor, regulated by proinflammatory stimuli, that destabilizes vascular endothelium and increases vascular leakage; consequently, Ang-2 may contribute to sepsis pathophysiology. We have studied 1) serum Ang-2 levels in critically-ill patients and investigated potential relationships with inflammatory mediators and indices of disease severity and 2) the effect of sepsis-related inflammatory mediators on Ang-2 production by lung endothelium in vitro. DESIGN: Prospective clinical study followed by cell culture studies. SETTING: General intensive care unit and research laboratory of a university hospital. SUBJECTS: Human and bovine lung microvascular endothelial cells and 61 patients (32 men). Patients were grouped according to their septic stage as having: no systemic inflammatory response syndrome (n = 6), systemic inflammatory response syndrome (n = 8), sepsis (n = 16), severe sepsis (n = 18), and septic shock (n = 13). INTERVENTIONS: Cells were exposed to lipopolysaccharide, tumor necrosis factor-alpha, and interleukin-6. MEASUREMENTS AND MAIN RESULTS: Patients' serum Ang-2 levels were significantly increased in severe sepsis as compared with patients with no systemic inflammatory response syndrome or sepsis (p < .05 by analysis of variance). Positive linear relationships were observed with: serum tumor necrosis factor-alpha (rs = 0.654, p < .001), serum interleukin-6 (rs = 0.464, p < .001), Acute Physiology and Chronic Health Evaluation II score (rs = 0.387, p < .001), and Sequential Organ Failure Assessment score (rs = 0.428, p < .001). Multiple regression analysis revealed that serum Ang-2 is mostly related to serum tumor necrosis factor-alpha and severe sepsis. Treatment of human lung microvascular endothelial cells with all mediators resulted in a concentration-dependent Ang-2 reduction. Treatment of bovine lung microvascular endothelial cells with lipopolysaccharide and tumor necrosis factor-alpha increased Ang-2 release, and interleukin-6 reduced basal Ang-2 levels. CONCLUSIONS: First, patients' serum Ang-2 levels are increased during severe sepsis and associated with disease severity. The strong relationship of serum Ang-2 with serum tumor necrosis factor-alpha suggests that the latter may participate in the regulation of Ang-2 production in sepsis. Second, inflammatory mediators reduce Ang-2 release from human lung microvascular endothelial cells, implying that this vascular bed may not be the source of increased Ang-2 in human sepsis.

APACHE↗
PubMed2006

Antioxidants increase the ventilatory response to hyperoxic hypercapnia.

RATIONALE: The mechanisms by which chemoreceptors process carbon dioxide stimuli are poorly understood. Recent in vitro studies suggest a role of reactive oxygen species in central carbon dioxide chemoreception. OBJECTIVES: We tested the hypothesis that antioxidant treatment modulates the ventilatory response to carbon dioxide in healthy humans, either during unloaded breathing or after strenuous resistive breathing. METHODS: In the first experiment of this randomized, double-blind, placebo-controlled study, 14 healthy males completed hyperoxic carbon dioxide rebreathing, received either antioxidants (vitamins E, A, and C for 2 mo, allopurinol for 15 d, and N-acetylcysteine for 3 d) (n = 7) or placebo (n = 7), and repeated rebreathing 3 mo later. In the second experiment, 18 healthy males completed a series of rebreathing tests before and after strenuous resistive breathing. Subjects repeated the same protocol 3 mo later, after they had received antioxidants (n = 9) or placebo (n = 9). MAIN RESULTS: After antioxidants, the sensitivity of the ventilatory (minute ventilation) response to carbon dioxide increased (mean [+/- SEM], 3.2 +/- 0.5 vs. 1.7 +/- 0.4 L/min/mm Hg; p < 0.001). Antioxidants also increased the sensitivity to carbon dioxide before and at 5, 30, and 120 min after resistive breathing (p = 0.01). This effect was entirely due to increased tidal volume. Antioxidants did not influence the breathing pattern during resting breathing or the rapid shallow breathing response to carbon dioxide at 5 min after resistive breathing. CONCLUSIONS: Antioxidants, by augmenting the tidal volume, increase the sensitivity of the ventilatory response to carbon dioxide, either during unloaded breathing or after resistive breathing.

Adult↗
PubMed2006

The combination of the load/force balance and the frequency/tidal volume can predict weaning outcome.

OBJECTIVE: To examine whether an appropriately designed combination of an index of ventilatory endurance and the frequency divided by tidal volume ratio (f/VT) provides prognostic information for weaning outcome not offered by any index alone. DESIGN AND SETTING: Prospective study in a multidisciplinary intensive care unit, university hospital. PATIENTS: 124 consecutive mechanically ventilated patients. INTERVENTIONS: We designed an index of ventilatory endurance (load/force balance) calculated as the mean inspiratory airway pressure (PI) during controlled mechanical ventilation/maximum inspiratory pressure (MIP) [PI equals the triplicate of mean airway pressure (Paw) displayed by the ventilator] and tested its capacity in predicting weaning outcome at 48 h along with f/VT and many other indices in 75 consecutive mechanically ventilated patients ready to wean. A stepwise discriminant function analysis was used to test the performance of appropriately designed index combination. Threshold values of indices and their combination were prospectively validated in another group of 45 consecutive patients. RESULTS: Stepwise discriminant analysis showed that PI/MIP and f/VT were the only indices that remained in the model with the function D=7.628xmean Paw/MIP+0.0158xf/VT-2.374. The cutoff point of D=0.5 had 94% sensitivity, 67% specificity, and 87% correct classifications. Prospective validation demonstrated similar results. The simplified discriminant function D=15xmean Paw/MIP+0.003xf/VT-5 and the cut-off point of D=1.0 had 89% sensitivity, 67% specificity, and 85% correct classifications. CONCLUSIONS: The combination of mean Paw/MIP and f/VT in a simplified discriminant function is useful in predicting weaning outcome.

Female↗
PubMed2006

Effects of exercise-induced arterial hypoxaemia and work rate on diaphragmatic fatigue in highly trained endurance athletes.

Diaphragmatic fatigue occurs in highly trained athletes during exhaustive exercise. Since approximately half of them also exhibit exercise-induced arterial hypoxaemia (EIAH) during high-intensity exercise, the present study sought to test the hypothesis that arterial hypoxaemia contributes to exercise-induced diaphragmatic fatigue in this population. Ten cyclists ( : 70.0 +/- 1.6 ml kg(-1) min(-1); mean +/-s.e.m.) completed, in a balanced ordering sequence, one normoxic (end-exercise arterial O(2) saturation (S(a,O(2))): 92 +/- 1%) and one hyperoxic (F(I,O(2)): 0.5% O(2); S(a,O(2)) : 97 +/- 1%) 5 min exercise test at intensities equal to 80 +/- 3 and 90 +/- 3% of maximal work rate (WR(max)), respectively, producing the same tidal volume (V(T)) and breathing frequency (f) throughout exercise. Cervical magnetic stimulation was used to determine reduction in twitch transdiaphragmatic pressure (P(di,tw)) during recovery. Hyperoxic exercise at 90% WR(max) induced significantly (P= 0.022) greater post-exercise reduction in P(di,tw) (15 +/- 2%) than did normoxic exercise at 80% WR(max) (9 +/- 2%), despite the similar mean ventilation (123 +/- 8 and 119 +/- 8 l min(-1), respectively), breathing pattern (V(T): 2.53 +/- 0.05 and 2.61 +/- 0.05 l, f: 49 +/- 2 and 46 +/- 2 breaths min(-1), respectively), mean changes in P(di) during exercise (37.1 +/- 2.4 and 38.2 +/- 2.8 cmH(2)O, respectively) and end-exercise arterial lactate (12.1 +/- 1.4 and 10.8 +/- 1.1 mmol l(-1), respectively). The difference found in diaphragmatic fatigue between the hyperoxic (at higher leg work rate) and the normoxic (at lower leg work rate) tests suggests that neither EIAH nor lactic acidosis per se are likely predominant causative factors in diaphragmatic fatigue in this population, at least at the level of S(a,O(2)) tested. Rather, this result leads us to hypothesize that blood flow competition with the legs is an important contributor to diaphragmatic fatigue in heavy exercise, assuming that higher leg work required greater leg blood flow.

Adult↗
PubMed2006

Regulation of Ang2 release by PTEN/PI3-kinase/Akt in lung microvascular endothelial cells.

Angiopoietin-2 (Ang2) is a Tie-2 ligand that destabilizes vascular structures, allowing for neovascularization or vessel regression depending on local vascular endothelial cell growth factor (VEGF) concentrations. Although various stimuli have been shown to affect Ang2 expression, information on the underlying mechanisms involved in Ang2 production in endothelial cells (EC) is just beginning to emerge. In the present study, we have used adenovirus-mediated gene transfer and pharmacological inhibitors to examine the role of the PTEN/PI3-K/Akt pathway on Ang2 release. Inhibition of PI3-kinase with wortmannin led to a stimulation of basal Ang2 release in EC, while overexpression of an active form of Akt reduced Ang2. In addition, adenovirus-mediated gene transfer of the phosphatase PTEN stimulated Ang2 release. Incubation of the cells with Ang1, an agent that activates the PI3-K/Akt pathway in EC, reduced Ang2 release. This effect of Ang1 could be prevented by wortmannin and LY-294002 pretreatment. Similarly, in VEGF-treated EC the increase in Ang2 production observed was greater in the presence of a PI3-K inhibitor. Our observations that PTEN acts as a positive modulator of Ang2 release, while activation of the PI3-K/Akt pathway downregulates Ang2, reveal an additional mechanism through which the PTEN/PI3-K/Akt pathway could affect the angiogenic process.

Androstadienes↗
PubMed2006

Bench-to-bedside review: weaning failure--should we rest the respiratory muscles with controlled mechanical ventilation?

The use of controlled mechanical ventilation (CMV) in patients who experience weaning failure after a spontaneous breathing trial or after extubation is a strategy based on the premise that respiratory muscle fatigue (requiring rest to recover) is the cause of weaning failure. Recent evidence, however, does not support the existence of low frequency fatigue (the type of fatigue that is long-lasting) in patients who fail to wean despite the excessive respiratory muscle load. This is because physicians have adopted criteria for the definition of spontaneous breathing trial failure and thus termination of unassisted breathing, which lead them to put patients back on the ventilator before the development of low frequency respiratory muscle fatigue. Thus, no reason exists to completely unload the respiratory muscles with CMV for low frequency fatigue reversal if weaning is terminated based on widely accepted predefined criteria. This is important, since experimental evidence suggests that CMV can induce dysfunction of the diaphragm, resulting in decreased diaphragmatic force generating capacity, which has been called ventilator-induced diaphragmatic dysfunction (VIDD). The mechanisms of VIDD are not fully elucidated, but include muscle atrophy, oxidative stress and structural injury. Partial modes of ventilatory support should be used whenever possible, since these modes attenuate the deleterious effects of mechanical ventilation on respiratory muscles. When CMV is used, concurrent administration of antioxidants (which decrease oxidative stress and thus attenuate VIDD) seems justified, since antioxidants may be beneficial (and are certainly not harmful) in critical care patients.

Animals↗
PubMed2005

Differential cardiovascular responses during weaning failure: effects on tissue oxygenation and lactate.

OBJECTIVE: To test the following two hypotheses during weaning failure: (a) mixed venous oxygen saturation (SvO2) does not decrease in patients whose oxygen consumption does not increase, and (b) blood lactate may increase in patients who demonstrate substantial decreases in SvO2. DESIGN AND SETTING: A prospective observational and physiological study in a 30-bed university intensive care unit. PATIENTS AND PARTICIPANTS: 18 patients who failed weaning and 12 patients who succeeded weaning (controls). MEASUREMENTS AND RESULTS: Hemodynamics, global tissue oxygenation, cardiovascular response (cardiac index/oxygen extraction diagram), and blood lactate were measured in ventilator-supported patients undergoing a spontaneous breathing trial. In patients who failed without having increased their oxygen consumption (n=9) the increase in oxygen delivery was accompanied by a decrease in oxygen extraction (by 15+/-4%). In patients who failed (n=9) having increased their oxygen consumption (by>10%) this increase was met mainly by an increase in oxygen extraction (by 30+/-7%). SvO2 increased by 2+/-1% in the former patients, whereas it decreased by 20+/-5% in the latter. Arterial lactate increased (range 2.3-3.1 mM/l) in only three patients who failed to have increased oxygen consumption and exhibited heart failure and the highest decreases in SvO2 (by 12-39%). CONCLUSIONS: Patients whose SvO2 does not decrease during weaning failure do not have increased oxygen consumption probably due to respiratory center depression in some of them. Patients whose SvO2 decreases have increased oxygen consumption.

Aged↗
PubMed2005

Both early-onset and late-onset ventilator-associated pneumonia are caused mainly by potentially multiresistant bacteria.

OBJECTIVE: To compare the causative pathogens of early-onset and late-onset ventilator-associated pneumonia (VAP) diagnosed by bronchoalveolar lavage quantitative cultures. Most previous reports have been based on endotracheal aspirate cultures and gave uncertain findings. DESIGN: Prospective evaluation of consecutive patients with clinical suspicion for VAP. SETTING: Multidisciplinary intensive care unit of a university hospital. PATIENTS AND PARTICIPANTS: During a 3-year period 473 patients with clinical suspicion of VAP entered the study. Diagnosis of VAP was confirmed by cultures of bronchoalveolar lavage (> 10(4) cfu/ml) specimens in 408 patients. INTERVENTIONS: Protected bronchoalveolar lavage samples were taken. Initial antibiotic therapy was modified upon bronchoalveolar lavage culture results. MEASUREMENTS AND RESULTS: Among 408 patients 191 had early-onset (< 7 days mechanical ventilation) and 217 late-onset (> or = 7 days) VAP. Potentially multiresistant bacteria, mainly Pseudomonas aeruginosa and methicillin-resistant Staphylococcus aureus (MRSA), were the most commonly isolated pathogens in both types of VAP. No difference was noted in the contribution of potentially multiresistant pathogens (79% vs. 85%), P. aeruginosa (42% vs. 47%), or MRSA (33% vs. 30%) between early-onset and late-onset VAP. Initial antibiotic therapy was modified in 58% of early-onset VAP episodes and in 36% of late-onset VAP episodes. No difference in mortality was found between the two types of VAP. CONCLUSIONS: Both early-onset and late-onset VAP were mainly caused by potentially multiresistant bacteria, most commonly P. aeruginosa and MRSA. Antimicrobial agents against these pathogens should be prescribed empirically, at least in our institution.

APACHE↗
PubMed2005

Anuria due to acute bilateral renal vein occlusion after thrombolysis for pulmonary embolism.

Severe hemorrhage is the more frequent complication of thrombolysis, with intracranial bleeding the most critical one. We report a 73-year-old woman with major pulmonary embolism (PE), yet haemodynamically stable, in whom thrombolysis resulted in severe complications with acute renal failure (ARF) due to bilateral renal vein occlusion, quite unexpected; this complication has never been reported, as yet. We believe that disrupture of peripheral vein clots by thrombolysis led to migration of thrombi particles upwards to the inferior vena cava (IVC) and bilateral renal vein occlusion. However, the large thrombus straddled to the bifurcation of the main pulmonary trunk and extending to the right pulmonary artery, as visualized by transthoracic (TTE) and transesophageal echocardiogram (TEE), was not affected by thrombolysis. Finally, endogenous fibrinolytic activity, under low molecular weight heparin, resulted in a slow dissolution of the pulmonary thrombus and restoration of kidney function.

Acute Disease↗
PubMed2005

Is loaded breathing an inflammatory stimulus?

PURPOSE OF REVIEW: To summarize recent data indicating that loaded breathing generates an inflammatory response. RECENT FINDINGS: Loaded breathing initiates an inflammatory response consisting of elevation of plasma cytokines and recruitment and activation of lymphocyte subpopulations. These cytokines do not originate from monocytes but are instead produced within the diaphragm secondary to the increased muscle activation. Oxidative stress is a major stimulus for the cytokine induction secondary to loaded breathing. The production of cytokines within the diaphragm may mediate the diaphragm muscle fiber injury that occurs with strenuous contractions, or contribute to the expected repair process. These cytokines may also compromise diaphragmatic contractility or contribute to the development of muscle cachexia. They may also have systemic effects, mobilizing glucose from the liver and free fatty acids from the adipose tissue to the strenuously working respiratory muscles. At the same time, they stimulate the hypothalamic-pituitary-adrenal axis, leading to the production of adrenocorticotropic hormone and beta-endorphins. The adrenocorticotropic hormone response may represent an attempt of the organism to reduce the injury occurring in the respiratory muscles through the production of glucocorticoids and the induction of the acute-phase response proteins. The beta-endorphin response would decrease the activation of the respiratory muscles and change the pattern of breathing, which becomes more rapid and shallow, possibly in an attempt to reduce and/or prevent further injury to the respiratory muscles. SUMMARY: Loaded breathing is an immune challenge for the body, initiating an inflammatory response. Further studies are needed to elucidate the role of this response in the development of ventilatory failure.

Airway Resistance↗
PubMed2005

Skeletal muscle adaptations to interval training in patients with advanced COPD.

STUDY OBJECTIVES: To investigate the response to interval exercise (IE) training by looking at changes in morphologic and biochemical characteristics of the vastus lateralis muscle, and to compare these changes to those incurred after constant-load exercise (CLE) training. DESIGN: Randomized, controlled, parallel, two-group study (IE vs CLE training). SETTING: Multidisciplinary, outpatient, hospital-based, pulmonary rehabilitation program. PATIENTS: Nineteen patients with stable advanced COPD (mean +/- SEM FEV1, 40 +/- 4% predicted). INTERVENTIONS: Patients (n = 10) assigned to IE training exercised at a mean intensity of 124 +/- 15% of baseline peak exercise capacity (peak work rate [Wpeak]) with 30-s work periods interspersed with 30-s rest periods for 45 min/d. Patients (n = 9) allocated to CLE training exercised at a mean intensity of 75 +/- 5% Wpeak for 30 min/d. Patients exercised 3 d/wk for 10 weeks. MEASUREMENTS AND RESULTS: Needle biopsies of the right vastus lateralis muscle were performed before and after rehabilitation. After IE training, the cross-sectional areas of type I and IIa fibers were significantly increased (type I before, 3,972 +/- 455 microm2; after, 4,934 +/- 467 microm2 [p = 0.004]; type IIa before, 3,695 +/- 372 microm2; after, 4,486 +/- 346 microm2 [p = 0.008]), whereas the capillary-to-fiber ratio was significantly enlarged (from 1.13 +/- 0.08 to 1.24 +/- 0.07 [p = 0.013]). Citrate synthase activity increased (from 14.3 +/- 1.4 to 20.5 +/- 4.2 micromol/min/g), albeit not significantly (p = 0.097). There was also a significant improvement in Wpeak (by 19 +/- 5%; p = 0.04) and in lactate threshold (by 17 +/- 5%; p = 0.02). The magnitude of changes in all the above variables was not significantly different compared to that incurred after CLE training. During training sessions, however, ratings of dyspnea and leg discomfort, expressed as fraction of values achieved at baseline Wpeak, were significantly lower (p < 0.05) for IE training (73 +/- 9% and 60 +/- 8%, respectively) compared to CLE training (83 +/- 10% and 87 +/- 13%, respectively). CONCLUSIONS: High-intensity IE training is equally effective to moderately intense CLE training in inducing peripheral muscle adaptations; however, IE is associated with fewer training symptoms.

Adaptation, Physiological↗
PubMed2002

Antioxidants attenuate the plasma cytokine response to exercise in humans.

Exercise increases plasma TNF-alpha, IL-1beta, and IL-6, yet the stimuli and sources of TNF-alpha and IL-1beta remain largely unknown. We tested the role of oxidative stress and the potential contribution of monocytes in this cytokine (especially IL-1beta) response in previously untrained individuals. Six healthy nonathletes performed two 45-min bicycle exercise sessions at 70% of Vo(2 max) before and after a combination of antioxidants (vitamins E, A, and C for 60 days; allopurinol for 15 days; and N-acetylcysteine for 3 days). Blood was drawn at baseline, end-exercise, and 30 and 120 min postexercise. Plasma cytokines were determined by ELISA and monocyte intracellular cytokine level by flow cytometry. Before antioxidants, TNF-alpha increased by 60%, IL-1beta by threefold, and IL-6 by sixfold secondary to exercise (P < 0.05). After antioxidants, plasma IL-1beta became undetectable, the TNF-alpha response to exercise was abolished, and the IL-6 response was significantly blunted (P < 0.05). Exercise did not increase the percentage of monocytes producing the cytokines or their mean fluorescence intensity. We conclude that in untrained humans oxidative stress is a major stimulus for exercise-induced cytokine production and that monocytes play no role in this process.

Acetylcysteine↗
PubMed2002

Strenuous resistive breathing induces plasma cytokines: role of antioxidants and monocytes.

Inspiratory resistive breathing increases plasma cytokines, yet the stimulus (or stimuli) and source(s) remain unknown. We tested the role of reactive oxygen species as stimuli and of monocytes as sources of resistive breathing-induced cytokines. Six healthy subjects performed two resistive breathing sessions at 75% of maximum inspiratory pressure before and after a combination of antioxidants (vitamin E 200 mg, vitamin A 50,000 IU, and vitamin C 1,000 mg per day for 60 days, allopurinol 600 mg/day for 15 days, and N-acetylcysteine 2 g/day for 3 days before the second session). Blood was drawn before, at the end, and at 30 and 120 minutes after resistive breathing. Before antioxidants, plasma cytokine levels (determined by enzyme-linked immunosorbent assay) increased secondary to resistive breathing (tumor necrosis factor-alpha and interleukin [IL]-6 by twofold and IL-1beta by threefold). After antioxidants, plasma IL-1beta became undetectable. The tumor necrosis factor-alpha response to resistive breathing was abolished, and the IL-6 response was significantly blunted. Intracellular cytokine detection (by flow cytometry) showed no change in either the percentage of monocytes producing the cytokines or their mean fluorescence intensity both before and after antioxidants. We conclude that oxidative stress is a major stimulus for the resistive breathing-induced cytokine production and that monocytes play no role in this process.

Adult↗
PubMed2002

Production of interleukin-6 by skeletal myotubes: role of reactive oxygen species.

In the present study we have tested the ability of reactive oxygen species (ROS) to stimulate the production of interleukin (IL)- 6 from skeletal myocytes. Differentiated C2C12 murine skeletal muscle cells (myotubes) exposed to pyrogallol (PYR), xanthine/ xanthine-oxidase (X/XO), or H(2)O(2) for 24 h exhibited a concentration-dependent increase in IL-6 production. Unlike myotubes, incubation of myoblasts and endothelial cells with X/XO or PYR did not result in increased IL-6 release. In myotubes, superoxide dismutase and catalase blocked the ROS-induced IL-6 release. Exposure of myotubes to H(2)O(2) increased steady-state IL-6 mRNA levels, and pretreatment of myotubes with actinomycin D or cycloheximide abolished the ROS-induced IL-6 production. In addition, pretreatment of cells with N-acetyl-cysteine blocked tumor necrosis factor (TNF)-alpha-induced IL-6 release, suggesting that endogenously produced ROS participate in IL-6 production. Myotubes stimulated with H(2)O(2) exhibited increased I kappa B-alpha phosphorylation and degradation, and treatment of C2C12 with ROS-generating agents increased activator protein (AP)-1 and nuclear factor (NF)-kappa B-dependent promoter activity. Finally, preincubation of myotubes with the pharmacologic inhibitor of NF-kappa B, diethyldithiocarbamate, or transient transfection with an I kappa B-alpha mutant, inhibited the ROS-stimulated IL-6 release. In conclusion, ROS stimulate IL-6 production from skeletal myotubes in a manner that involves transcriptional activation of the IL-6 gene through an NF-kappa B-dependent pathway.

Animals↗
PubMedDate not supplied

Hemorrhagic cardiac tamponade in critically ill patients with acute renal failure.

PURPOSE: The purpose of this study was to report the development, management, and follow up of tamponading uremic pericardial effusion in critically ill patients with acute renal failure. SETTING: The setting for this study was an adult, 24-bed tertiary multidisciplinary intensive care unit (ICU) of a university hospital. PATIENTS: The subjects were 5 critically ill patients with multiple organ failure including acute renal failure (ARF) that was slow to resolve. RESULTS: Renal involvement was attributed to renal hypoperfusion, sepsis and myoglobinuria. Continuous veno-venous hemofiltration (CVVH) was instituted early during hospitalization in 4 cases and lasted for 35 to 48 days; renal replacement therapy was not used in 1 case. Tamponade developed late in the course of ARF, after CVVH was discontinued in the 4 cases and was effectively managed with percutaneous pericardiocentesis under echocardiography and continuous catheter drainage of the pericardial sac for 48 to 72 hours. Hemorrhagic fluid (Hb 2.2-5.9 g/dL) with lymphocyte predominance was detected. Transient constrictive-like pericarditis findings were present in all patients after the procedure. All patients were discharged from the hospital in a good condition with normal serum and creatinine levels; 1-year follow up showed a normal echocardiogram. CONCLUSION: Awareness for the possibility of hemorrhagic pericarditis and cardiac tamponade is needed in ICU patients with ARF slow to resolve. Transient constrictive-like pericarditis may present after pericardiocentesis.

Acute Kidney Injury↗