Skills among young and elderly laypersons during simulated dispatcher assisted CPR and after CPR training.

BACKGROUND: Dispatcher assisted cardiopulmonary resuscitation (DA-CPR) increase the rate of bystander CPR. The aim of the study was to compare the performance of DA-CPR and attainable skills following CPR training between young and elderly laypersons. METHODS: Volunteer laypersons (young: 18-40 years; elderly: > 65 years) participated. Single rescuer CPR was performed in a simulated DA-CPR cardiac arrest scenario and after CPR training. Data were obtained from a manikin and from video recordings. The primary endpoint was chest compression depth. RESULTS: Overall, 56 young (median age: 26, years since last CPR training: 6) and 58 elderly (median age: 72, years since last CPR training: 26.5) participated. Young laypersons performed deeper (mean (SD): 56 (14) mm vs. 39 (19) mm, P < 0.001) and faster (median (25th-75th percentile): 107 (97-112) per min vs. 84 (74-107) per min, P < 0.001) chest compressions compared to elderly. Young laypersons had shorter time to first compression (mean (SD): 71 (11) seconds vs. 104 (38) seconds, P < 0.001) and less hands-off time (median (25th-75th percentile): 0 (0-1) seconds vs. 5 (2-10) seconds, P < 0.001) than elderly. After CPR training chest compressions were performed with a depth (mean (SD): 64 (8) mm vs. 50 (14) mm, P < 0.001) and rate (mean (SD): 111 (11) per min vs. 93 (18) per min, P < 0.001) for young and elderly laypersons respectively. CONCLUSION: Despite long CPR retention time for both groups, elderly laypersons had longer retention time, and performed inadequate DA-CPR compared to young laypersons. Following CPR training the attainable CPR level was of acceptable quality for both young and elderly laypersons.

2017 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations Summary

The International Liaison Committee on Resuscitation has initiated a near-continuous review of cardiopulmonary resuscitation science that replaces the previous 5-year cyclic batch-and-queue approach process. This is the first of an annual series of International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations summary articles that will include the cardiopulmonary resuscitation science reviewed by the International Liaison Committee on Resuscitation in the previous year. The review this year includes 5 basic life support and 1 pediatric Consensuses on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Each of these includes a summary of the science and its quality based on Grading of Recommendations, Assessment, Development, and Evaluation criteria and treatment recommendations. Insights into the deliberations of the International Liaison Committee on Resuscitation task force members are provided in Values and Preferences sections. Finally, the task force members have prioritized and listed the top 3 knowledge gaps for each population, intervention, comparator, and outcome question

Reduced right ventricular diameter during cardiac arrest caused by tension pneumothorax - a porcine ultrasound study.

INTRODUCTION: Advanced life support (ALS) guidelines recommend ultrasound to identify reversible causes of cardiac arrest. Right ventricular (RV) dilatation during cardiac arrest is commonly interpreted as a sign of pulmonary embolism. The RV is thus a focus of clinical ultrasound examination. Importantly, in animal studies ventricular fibrillation and hypoxia results in RV dilatation. Tension pneumothorax (tPTX) is another reversible cause of cardiac arrest, however, the impact on RV diameter remains unknown. AIM: To investigate RV diameter evaluated by ultrasound in cardiac arrest caused by tPTX or hypoxia. METHODS: Pigs were randomized to cardiac arrest by either tPTX (n = 9) or hypoxia (n = 9) and subsequently resuscitated. Tension pneumothorax was induced by injection of air into the pleural cavity. Hypoxia was induced by reducing tidal volume. Ultrasound images of the RV were obtained throughout the study. Tension pneumothorax was decompressed after the seventh rhythm analysis. The primary endpoint was RV diameter after the third rhythm analysis. RESULTS: At cardiac arrest the RV diameter was 17 mm (95% CI: 13; 21) in the tPTX group and 36 mm (95% CI: 33; 40) in the hypoxia group (P < 0.01, n = 9 for both). At third rhythm analysis RV diameter was smaller in the tPTX group: 12 mm (95% CI: 7; 16) vs. hypoxia group: 28 mm (25; 32) (P < 0.01). After decompression no difference existed between groups: tPTX 29 mm (95% CI: 23; 34) vs. hypoxia 29 mm (95% CI: 20; 38). CONCLUSION: The RV diameter is smaller during cardiopulmonary resuscitation in cardiac arrest caused by tPTX when compared with hypoxia. The difference disappears after tPTX decompression.

A randomised crossover comparison of mouth-to-face-shield ventilation and mouth-to-pocket-mask ventilation by surf lifeguards in a manikin.

Thirty surf lifeguards (mean (SD) age: 25.1 (4.8) years; 21 male, 9 female) were randomly assigned to perform 2 × 3 min of cardiopulmonary resuscitation on a manikin using mouth-to-face-shield ventilation (AMBU LifeKey) and mouth-to-pocket-mask ventilation (Laerdal Pocket Mask). Interruptions in chest compressions, effective ventilation (visible chest rise) ratio, tidal volume and inspiratory time were recorded. Interruptions in chest compressions per cycle were increased with mouth-to-face-shield ventilation (mean (SD) 8.6 (1.7) s) compared with mouth-to-pocket-mask ventilation (6.9 (1.2) s, p < 0.0001). The proportion of effective ventilations was less using mouth-to-face-shield ventilation (199/242 (82%)) compared with mouth-to-pocket-mask ventilation (239/240 (100%), p = 0.0002). Tidal volume was lower using mouth-to-face-shield ventilation (mean (SD) 0.36 (0.20) l) compared with mouth-to-pocket-mask ventilation (0.45 (0.20) l, p = 0.006). No differences in inspiratory times were observed between mouth-to-face-shield ventilation and mouth-to-pocket-mask ventilation. In conclusion, mouth-to-face-shield ventilation increases interruptions in chest compressions, reduces the proportion of effective ventilations and decreases delivered tidal volumes compared with mouth-to-pocket-mask ventilation.

A randomised crossover comparison of manikin ventilation through Soft Seal®, i-gel™ and AuraOnce™ supraglottic airway devices by surf lifeguards.

Forty surf lifeguards attempted to ventilate a manikin through one out of three supraglottic airways inserted in random order: the Portex® Soft Seal®; the Intersurgical® i-gel™; and the Ambu® AuraOnce™. We recorded the time to ventilate and the proportion of inflations that were successful, without and then with concurrent chest compressions. The mean (SD) time to ventilate with the Soft Seal, i-gel and AuraOnce was 35.2 (7.2)s, 15.6 (3.3)s and 35.1 (8.5) s, respectively, p < 0.0001. Concurrent chest compression prolonged the time to ventilate by 5.0 (1.3-8.1)%, p = 0.0072. The rate of successful ventilations through the Soft Seal (100%) was more than through the AuraOnce (92%), p < 0.0001, neither of which was different from the i-gel (97%). The mean (SD) tidal volumes through the Soft Seal, i-gel and AuraOnce were 0.65 (0.14) l, 0.50 (0.16) l and 0.39 (0.19) l, respectively. Most lifeguards (85%) preferred the i-gel. Ventilation through supraglottic airway devices may be considered for resuscitation by surf lifeguards.

Exercise-induced cardioprotection is mediated by a bloodborne, transferable factor.

Exercise protects against myocardial ischemia-reperfusion (I-R) injury but the mechanism remains unclear. Protection can be transferred from a remotely preconditioned human donor to an isolated perfused rabbit heart using a dialysate of plasma. We hypothesized that physical exercise preconditioning also confers cardioprotection through a humorally mediated effector dependent on opioid receptor activation. Thirteen male volunteers performed vigorous exercise (four 2-minute bouts of high-intensity exercise) and 1 week later they underwent remote ischemic preconditioning (four cycles of 5 min upper limb ischemia and reperfusion). Dialysates were prepared from blood collected before (control) and after the two interventions. Isolated rabbit hearts were perfused with the dialysates without and with co-administration of naloxone (opioid receptor antagonist) prior to 40 min regional ischemia and 2 h reperfusion. Exercise and remote ischemic preconditioning (rIPC) reduced infarct size from 60 ± 5 to 35 ± 5 % and from 57 ± 7 to 27 ± 3 % of the area at risk, respectively (p < 0.05 and < 0.01). Furthermore, post-ischemic left ventricular developed pressure was improved compared with controls (p = 0.08 for exercise and p = 0.04 for rIPC). Co-perfusion with naloxone abrogated the protective effects of exercise and remote ischemic preconditioned dialysates. In conclusion, high-intensity exercise preconditioning elicits cardioprotection through a humorally mediated dependent on opioid receptor activation, similar to rIPC.

Comparison of two sulfonylureas with high and low myocardial K(ATP) channel affinity on myocardial infarct size and metabolism in a rat model of type 2 diabetes.

AIMS/HYPOTHESIS: Sulfonylureas (SUs) may impair outcome in patients with acute coronary syndrome. Most experimental studies of the myocardial effects of SU treatment are performed in non-diabetic models. We compared the effect of two widely used SUs, glibenclamide (gb) and gliclazide (gc), with high and low myocardial K(ATP) channel affinity, respectively, at therapeutic concentrations on infarct size, left ventricular (LV) function and myocardial glycogen, lactate and alanine content before and after ischaemia/reperfusion (I/R). METHODS: Non-diabetic Wistar and diabetic Goto-Kakizaki rat hearts were investigated in a Langendorff preparation. Gb (0.1 µmol/l) and gc (1.0 µmol/l) were administrated throughout the study. Infarct size was evaluated after 120 min of reperfusion. Myocardial metabolite content was measured before and after ischaemia. RESULTS: Infarct size was smaller in diabetic hearts than in non-diabetic hearts (0.33 ± 0.03 vs 0.51 ± 0.05, p < 0.05). Gb increased infarct size (0.54 ± 0.04 vs 0.33 ± 0.03, p < 0.05) and reduced post-ischaemic LV developed pressure (60 ± 3 vs 76 ± 3 mmHg, p < 0.05) and coronary flow (4.9 ± 0.5 vs 7.1 ± 0.4 ml min(-1) g(-1), p < 0.05) in gb-treated diabetic rats compared with untreated diabetic rats. On comparing gb-treated diabetic rats with untreated diabetic rats, glycogen content was reduced before (9.1 ± 0.6 vs 13.6 ± 1.0 nmol/mg wet weight, p < 0.01) and after ischaemia (0.9 ± 0.2 vs 1.8 ± 0.2 nmol/mg wet weight, p < 0.05), and lactate (4.8 ± 0.4 vs 3.2 ± 0.3 nmol/mg wet weight, p < 0.01) and alanine (1.38 ± 0.12 vs 0.96 ± 0.09 nmol/mg wet weight, p < 0.05) contents were increased during reperfusion. Gc-treatment of diabetic and non-diabetic rats did not affect any of the measured variables. CONCLUSIONS/INTERPRETATIONS: Gb, but not gc, exacerbates I/R injury and deteriorates LV function in diabetic hearts. These effects of gb on diabetic hearts may be due to detrimental effects on myocardial carbohydrate metabolism.

Cardioprotective effect of L-glutamate in obese type 2 diabetic Zucker fatty rats.

1. Because diabetic hearts have an increased threshold for cardioprotection by ischaemic preconditioning (IPC), we hypothesized that protection by L-glutamate during reperfusion is restricted in Type 2 diabetic hearts. Previously, we found that L-glutamate-mediated postischaemic cardioprotection mimics IPC. 2. Rat hearts were studied in a Langendorff preparation perfused with Krebs'-Henseleit solution and subjected to 40 min global no-flow ischaemia, followed by 120 min reperfusion. L-Glutamate (0, 15 and 30 mmol/L) was added to the perfusate during reperfusion of hearts from non-diabetic (Wistar-Kyoto) and diabetic (Zucker diabetic fatty (ZDF)) rats, studied at 16 weeks of age. The infarct size (IS)/area-at-risk (AAR) ratio was the primary end-point. Expression of L-glutamate excitatory amino acid transporter (EAAT) 1 (mitochondrial) and EAAT3 (sarcolemmal) was determined by quantitative polymerase chain reaction and immunoblotting. 3. The ISS/AAR ratio did not differ between control hearts from Wistar-Kyoto and ZDF rats (0.52 ± 0.03 and 0.51 ± 0.04, respectively; P = 0.90). L-Glutamate (15 mmol/L) significantly reduced the IS/AAR ratio in non-diabetic hearts, but not in diabetic hearts, compared with their respective controls. The higher concentration of L-glutamate (30 mmol/L) reduced infarct size in diabetic hearts to the same degree as in non-diabetic hearts (IS/AAR 0.35 ± 0.03 (P = 0.002) and 0.34 ± 0.03 (P = 0.004), respectively). The mitochondrial L-glutamate transporter EAAT1 was downregulated in hearts from ZDF rats at both the mRNA and protein levels (P < 0.0005 and P < 0.0001, respectively). However, there was no change in EAAT3 expression at the protein level. Myocardial L-glutamate content was increased by 43% in diabetic hearts (P < 0.0001). 4. Hearts from obese diabetic rats have an elevated threshold for metabolic postischaemic cardioprotection by L-glutamate. These findings may reflect underlying mechanisms of inherent resistance against additional cardioprotection in the diabetic heart.

Validation of a fall risk index in stroke rehabilitation.

A fall risk index has previously been developed to identify fall-prone individuals in stroke rehabilitation. The purpose of this study was to validate the predictive accuracy of the index. The validation sample (n = 158) consisted of patients admitted to a specialized geriatric stroke rehabilitation ward. The index was scored for each subject, and the relationship between the score and falls was assessed. The index was then remodeled and cross-validated in the sample from which it was derived (model fit sample, n = 135). The total index score (0-11) was significantly connected with the time to first fall (hazard ratio, 1.22; confidence interval [CI], 1.03-1.44). However, the classification of subjects into groups with low, intermediate, and high risk of falling could not be correlated with the time to first fall. A remodeled index contained 3 of the separate original index items. Its relationship to fall risk in the model fit sample was (hazard ratio, 1.82; CI, 1.38-2.40). The fall risk index showed some correlation with the fall risk among patients in stroke rehabilitation, but the results indicate that it should be modified to reach acceptable accuracy. A remodeled index showed a higher association with fall risk.

Ischaemic preconditioning does not protect the heart in obese and lean animal models of type 2 diabetes.

AIMS/HYPOTHESIS: The prevalence of type 2 diabetes mellitus is increasing worldwide with obese diabetic patients constituting the majority of this population. Type 2 diabetes is associated with increased morbidity and mortality after acute myocardial infarction. Previous experimental studies of ischaemia-reperfusion tolerance in diabetes have only been performed in animal models of type 1 diabetes mellitus, yielding conflicting data. The aim of the present study was to characterise and compare the tolerance to ischaemia and effects of ischaemic preconditioning (IPC) in hearts from obese Zucker diabetic fatty (ZDF) and lean Goto-Kakizaki (GK) type 2 diabetic rats, using non-obese Zucker and Wistar rats as respective controls. METHODS: The two rat strains were divided into 8 groups. The ZDF study (n=47) consisted of: Control -IPC, Control +IPC, ZDF -IPC and ZDF +IPC. The GK study (n=38) consisted of: Control -IPC, Control +IPC, GK -IPC and GK +IPC. Hearts, which were studied in a Langendorff preparation perfused with Krebs-Henseleit buffer, were subjected or not to IPC (+IPC, -IPC) before 50 minutes of regional ischaemia and 120 minutes reperfusion. RESULTS: Ischaemic reperfusion injury was smaller in obese (p<0.05) and lean (p<0.05) type 2 diabetic animals than in their respective control animals. IPC reduced ischaemic reperfusion injury during reperfusion in non-diabetic control rats (p<0.01), but failed to protect hearts from both diabetic animal models. Post-ischaemic haemodynamic recovery was impaired in the ZDF rats compared to both control and GK rats (p<0.05). CONCLUSIONS/INTERPRETATION: Ischaemic preconditioning does not protect hearts from obese or lean type 2 diabetic animals. However, the susceptibility of the type 2 diabetic myocardium to ischaemic damage is lower than in non-diabetic hearts. The method described here could be used as a tool to study the pathogenesis of increased cardiovascular morbidity and mortality in type 2 diabetes.

Cross-validation of a model predicting discharge home after stroke rehabilitation. Validating stroke discharge predictors.

A new sample of 116 stroke patients was collected in order to validate a logistic regression model, predicting the chances of severely affected stroke patients being discharged home to independent living. The model was found to be accurate in the new sample, especially for those patients who had a high estimated probability of being discharged home. When the dividing line for the predicted probability for discharge home was set at a value of >/=0.5, the positive and negative predictive values were 74 and 73%, respectively. Further modelling resulted in a new extended model including the variables postural stability on admission, cohabiting, age and perceptual impairment on admission that formed the basis for an index predicting discharge home. This index was then validated in the sample of 93 patients that the first developed model was derived from and showed positive and negative predictive values of 85 and 77%, respectively.

PKCepsilon, via its regulatory domain and independently of its catalytic domain, induces neurite-like processes in neuroblastoma cells.

To investigate the role of protein kinase C (PKC) isoforms in regulation of neurite outgrowth, PKCalpha, betaII, delta, and epsilon fused to enhanced green fluorescent protein (EGFP) were transiently overexpressed in neuroblastoma cells. Overexpression of PKCepsilon-EGFP induced cell processes whereas the other isoforms did not. The effect of PKCepsilon-EGFP was not suppressed by the PKC inhibitor GF109203X. Instead, process formation was more pronounced when the regulatory domain was introduced. Overexpression of various fragments from PKCepsilon regulatory domain revealed that a region encompassing the pseudosubstrate, the two C1 domains, and parts of the V3 region were necessary and sufficient for induction of processes. By deleting the second C1 domain from this construct, a dominant-negative protein was generated which suppressed processes induced by full-length PKCepsilon and neurites induced during retinoic acid- and growth factor-induced differentiation. As with neurites in differentiated neuroblastoma cells, processes induced by the PKCepsilon- PSC1V3 protein contained alpha-tubulin, neurofilament-160, and F-actin, but the PKCepsilon-PSC1V3-induced processes lacked the synaptic markers synaptophysin and neuropeptide Y. These data suggest that PKCepsilon, through its regulatory domain, can induce immature neurite-like processes via a mechanism that appears to be of importance for neurite outgrowth during neuronal differentiation.

Three years after in-patient stroke rehabilitation: A follow-up study.

A 3-year follow-up study was performed aimed at describing the outcome for severely affected stroke survivors who had undergone geriatric in-patient rehabilitation. Living conditions, psychological well-being, and changes in functions were assessed in 55 survivors. Twenty-five people were living in the community, 15 in apartment hotels or homes for the aged and 15 in nursing homes. From discharge to follow-up 11 people had had to move to an accommodation offering more support. Living alone, recurrent strokes and functional decline were associated with moving. Many of those living in the community were supported by relatives or home help services. Home adjustments and assistive devices were common and in most cases were aimed at facilitating transfers and bathroom activities. Motor function had deteriorated from discharge to follow-up, otherwise no statistically significant changes were seen in the survivors' abilities and functions. Most survivors had in fact been able to maintain their functions or to make further improvements. Also, their psychological well-being seemed quite good. These results should encourage rehabilitation efforts for elderly people severely affected by stroke.

Psychological well-being 3 years after severe stroke.

BACKGROUND AND PURPOSE: Stroke often has a very negative influence on the victims' perception of their life situation. The aim of this study was therefore to assess the subjects' long-term psychological well-being and to explore associations between subject characteristics, impairments, disabilities, and psychological well-being. METHODS: Of 100 subjects rehabilitated at a specialized geriatric stroke ward after the acute phase, 47 survivors were assessed in their homes 3 years after discharge and interviewed regarding their psychological well-being with the Philadelphia Geriatric Center Morale Scale (PGCMS). RESULTS: Sixty-four percent of the subjects were classified as having high scores for psychological well-being or fell within the middle range. In a cluster analysis, depression was shown to have the strongest association with the subjects' PGCMS scores. Variables including the subjects' social situation and functions as well as age, gender, ability to communicate, and need for help showed a much weaker association with the PGCMS. CONCLUSIONS: More than half of the stroke subjects were classified as having levels of psychological well-being that were good or fairly good. The strong association between PGCMS scores and depression indicates the importance of detecting and treating depression and of following up initiated therapy after stroke.

In-patient rehabilitation after stroke: outcome and factors associated with improvement.

A study aimed at examining the outcome of activities of daily living (ADL) of patients undergoing geriatric stroke rehabilitation was performed. Background and admission data of 99 patients surviving the acute phase and needing further hospital rehabilitation were registered. Forty per cent of the patients improved their ADL ability. The logistic regression modelling with the dichotomous dependent variable improvement versus no improvement showed the following factors associated with improvement: a diagnosis of intracerebral haemorrhage, male sex, high postural stability score at the admission and cohabitation. In conclusion, the most severely affected stroke patients, especially patients with intracerebral haemorrhage, have a great potential for improving their ADL. The results of the logistic regression model can serve as a useful guide when it comes to identifying patients that stand a fair chance of improving during their rehabilitation stay. Equally important, patients with a poor rehabilitation prognosis who may need intensified rehabilitation efforts to achieve optimum improvement can now be identified.

Inhibition of human and duck hepatitis B virus by 2',3'-dideoxy-3'-fluoroguanosine in vitro.

The fluorinated guanosine analog 2',3'-dideoxy-3'-fluoroguanosine (FLG) has been shown to have an effect on duck hepatitis B virus (DHBV) in vivo and in vitro. In this study the inhibitory effect of FLG on DHBV and human hepatitis B virus (HBV) was evaluated in vitro. Cell lines transfected either with DHBV or HBV DNA and primary duck hepatocyte cell cultures were used. Virus production was analysed by PCR and a quantitative PCR was established for DHBV for determination of the inhibitory concentrations of the drug. 50% inhibition was achieved with an FLG concentration of 0.2 microg/ml (0.7 microM) and 90% inhibition was observed with an FLG concentration of 1.0 microg/ml (3.7 microM) using the DHBV transfected cell line. FLG showed an effect on DHBV production in primary duck hepatocyte cell cultures at concentrations down to 0.1 microg/ml (0.4 microM). However, the DHBV production returned to pre-treatment levels within a few days after cessation of treatment. HBV production in transfected cell lines was also inhibited by FLG. Both DHBV and HBV DNA-polymerases were inhibited by FLG triphosphate and 50% inhibition was observed at a concentration of 0.05 microg/ml (0.1 microM) for DHBV and 0.03 microg/ml (0.05 microM) for HBV. FLG is an efficient inhibitor of DHBV replication both in vivo and in vitro and of HBV in vitro which makes it a good candidate for treatment of HBV infections. However, it does not completely eliminate the virus since a relapse in virus production was observed when treatment was withdrawn. Therefore it would be interesting to evaluate FLG in combination with other types of anti-HBV drugs.

2',3'-dideoxy-3'-fluoroguanosine inhibits duck hepatitis B virus in vivo.

Duck hepatitis B virus (DHBV) belongs to the same virus family as the human hepatitis B virus (HBV). Domestic ducks infected with DHBV can be used as an animal model for chronic hepatitis B virus infection in therapeutic trials. In this study the antiviral effect of the guanosine analogue 2',3'-dideoxy-3'-fluoroguanosine (FLG) was tried in vivo on chronically DHBV-infected ducks. The ducks were either congenitally infected, or inoculated with DHBV immediately post-hatch. FLG was given as intraperitoneal injections twice daily, at different dosages. Serum DHBV levels were determined by DNA dot-blot hybridization. A strong inhibition of serum DHBV DNA was observed with FLG doses down to 1 mg kg-1 day-1, given for 7 to 10 days. With the corresponding thymidine analogue, 2',3'-dideoxy-3'-fluorothymidine; however, no inhibition was obtained. This difference may be due to different phosphorylation mechanisms. Independently of FLG dose, serum DHBV DNA returned to pretreatment levels within a few days after cessation of therapy. After a long-term trial (FLG, 5 mg kg-1 day-1 for 33 days), the same relapse of DHBV production was seen. Thus, FLG is an efficient inhibitor of DHBV replication, and is a candidate for treatment of HBV infections. However, the effect is transient, and therefore combination with other types of anti-HBV drugs should be considered.

Hepatitis C virus infection in hemodialysis patients in southern Sweden: epidemiological, clinical, and diagnostic aspects.

A prevalence of hepatitis C virus (HCV) antibodies of 12% was found in 276 patients from 11 dialysis units. Between zero and 22% of the patients in the different units were anti-HCV positive. The epidemiology of HCV was studied in two units during a 2 year period by antibody assays and the polymerase chain reaction and correlated with clinical manifestations. Two types of epidemiologic patterns were found that may explain the wide difference of HCV prevalence described in different dialysis units. In one unit there was no evidence of spread within the unit, and the prevalence of HCV was dependent on the status of the patients entering for treatment. In the other unit, a clustering of infected patients could be seen in which 13 of 36 were infected during a 3 year period. Some patients who had not received blood transfusions were among the infected. Hepatitis C infection was the most common explanation for repeated abnormal transferase levels. Most of the HCV-infected patients reacted both for anti-HCV and HCV RNA. HCV RNA was in general detected earlier than anti-HCV seroconversion. Among 20 HCV RNA-positive serum samples that were anti-HCV ELISA-positive 18 had indeterminate and two negative reactions by immunoblot (RIBA 2). Thus the RIBA 2 test should be used with caution as a confirmatory antibody test in this group of patients.