Effects of dialysis modality on blood loss, bleeding complications and transfusion requirements in critically ill patients with dialysis-dependent acute renal failure.

Blood loss and bleeding complications may often be observed in critically ill patients on renal replacement therapies (RRT). Here we investigate procedural (i.e. RRT-related) and non-procedural blood loss as well as transfusion requirements in regard to the chosen mode of dialysis (i.e. intermittent haemodialysis [IHD] versus continuous veno-venous haemofiltration [CVVH]). Two hundred and fifty-two patients (122 CVVH, 159 male; aged 61.5±13.9 years) with dialysis-dependent acute renal failure were analysed in a sub-analysis of the prospective randomised controlled clinical trial-CONVINT-comparing IHD and CVVH. Bleeding complications including severity of bleeding and RRT-related blood loss were assessed. We observed that 3.6% of patients died related to severe bleeding episodes (between group P=0.94). Major all-cause bleeding complications were observed in 23% IHD versus 26% of CVVH group patients (P=0.95). Under CVVH, the rate of RRT-related blood loss events (57.4% versus 30.4%, P=0.01) and mean total blood volume lost was increased (222.3±291.9 versus 112.5±222.7 ml per patient, P <0.001). Overall, transfusion rates did not differ between the study groups. In patients with sepsis, transfusion rates of all blood products were significantly higher when compared to cardiogenic shock (all P <0.01) or other conditions. In conclusion, procedural and non-procedural blood loss may often be observed in critically ill patients on RRT. In CVVH-treated patients, procedural blood loss was increased but overall transfusion rates remained unchanged. Our data show that IHD and CVVH may be regarded as equivalent approaches in critically ill patients with dialysis-dependent acute renal failure in this regard.

[Adsorption therapy in sepsis]. / Adsorbertherapie bei Sepsis.

BACKGROUND: The activation of multiple pro- and anti-inflammatory mediators is a key feature in the pathophysiology of sepsis. Many of these mediators may directly contribute to organ dysfunction and determine disease severity. So far our ability to modulate these upregulated mediator pathways is very limited. Therefore the adsorption of such mediators via an extracorporeal circuit may be a beneficial intervention during sepsis. OBJECTIVES: Recent technical innovations have made this intervention feasible. Both systems for exclusive mediator adsorption and for adsorption beside a conventional renal replacement therapy are now available. Some of the membranes can adsorb a broad range of mediators by rather unspecific binding, whereas others specifically adsorb endotoxin or mediators. DISCUSSION: Whilst biochemical efficacy could be demonstrated by some of the systems, controlled and randomized studies demonstrating improved clinical endpoints are still lacking. Therefore the use of such therapies outside clinical studies cannot yet be recommended.

Tympanic temperature during therapeutic hypothermia.

OBJECTIVE: Prehospital induction of therapeutic hypothermia after cardiac arrest may require temperature monitoring in the field. Tympanic temperature is non-invasive and frequently used in clinical practice. Nevertheless, it has not yet been evaluated in patients undergoing mild therapeutic hypothermia (MTH). Therefore, a prospective observational study was conducted comparing three different sites of temperature monitoring during therapeutic hypothermia. METHODS: Ten consecutive patients admitted to our medical intensive care unit after out-of-hospital cardiac arrest were included in this study. During MTH, tympanic temperature was measured using a digital thermometer. Simultaneously, oesophageal and bladder temperatures were recorded in a total of 558 single measurements. RESULTS: Compared with oesophageal temperature, bladder temperature had a bias of 0.019°C (limits of agreement ± 0.61°C (2SD)), and tympanic measurement had a bias of 0.021°C (± 0.80°C). Correlation analysis revealed a high relationship for tympanic versus oesophageal temperature (r = 0.95, p < 0.0001) and also for tympanic versus bladder temperature (r = 0.96, p < 0.0001). CONCLUSIONS: That tympanic temperature accurately indicates both oesophageal and bladder temperatures with a very small discrepancy in patients undergoing MTH after cardiac arrest is demonstrated in this study. Although our results were obtained in the hospital setting, these findings may be relevant for the prehospital application of therapeutic hypothermia as well. In this case, tympanic temperature may provide an easy and non-invasive method for temperature monitoring.

Immediate recovery of renal function after orthotopic liver transplantation in a patient with hepatorenal syndrome requiring hemodialysis for more than 8 months.

Severe liver dysfunction may lead to impairment of renal function without an underlying renal pathology. This phenomenon is called hepatorenal syndrome (HRS), which is associated with a poor prognosis showing a median survival of less than 2 months if renal replacement therapy is necessary. Liver transplantation is the best therapeutic option to regain renal function, but because of poor survival, these patients often die before transplantation. Herein we report a 37-year-old patient with ethyl-toxic liver cirrhosis who underwent hemodialysis due to HRS type I for more than 8 months. After living donor liver transplantation, diuresis immediately resumed, renal function soon recovered, and intermittent hemodialysis was stopped at 18 days after transplantation. Renal function was stable with a serum creatinine <2 mg/dL during the last 5 years posttransplantation. As far as we know, only a few cases of an anuric patient suffering from HRS have been reported with a survival beyond 8 months and full recovery of renal function after liver transplantation. This underlined that renal replacement therapy in HRS should be considered as a possible bridging method to liver transplantation even for longer periods.

Extensive coronary thrombosis in thrombotic-thrombocytopenic purpura.

We describe a case of a 41-year-old female patient who was admitted with typical signs of thrombotic-thrombocytopenic purpura. Markers of myocardial ischemia (Troponin T, CK, CK-MB) were even present at admission without symptoms of angina pectoris. Only a few hours after admission the patient developed all signs of cardiogenic shock with subsequently cardiac arrest. Postmortal coronary angiographies showed occlusions in all coronary arteries with significant myocardial necrosis. We are unaware of any report that describes macrovascular occlusions in thrombotic-thrombocytopenic purpura.

[60 year old patient with soft tissue infection of the right leg]. / 60-jähriger Patient mit Weichteilinfektion des rechten Beines.

Group A streptococcal necrotizing fasciitis is a rare disease associated with high mortality. Since severe toxic shock syndrome is a common complication, only immediate and aggressive surgical intervention, adequate antimicrobial therapy and supportive intensive care can be life-saving. We report about successful treatment of a 60-year old patient with necrotizing fasciitis and multiple organ failure.

Systemic inflammation in patients with heart failure.

AIMS: We hypothesized that chronic heart failure as a model of systemic hypoxia may result in systemic inflammation. The signs of a systemic inflammatory response should disappear after successful mechanical circulatory support using biventricular assist device systems. METHODS AND RESULTS: Plasma levels of cytokines (IL-6, IL-8, TNF-alpha) and soluble adhesion molecules (sVCAM, sE-, sL-, sP-Selectin) were determined in samples obtained from patients with chronic heart failure NYHA classes II-III, patients with overt cardiogenic shock before and after implantation of a mechanical assist-device system ('Berlin Heart') and in patients with coronary artery disease as a control. Elevated levels of cytokines and soluble adhesion molecules could be observed in patients with cardiogenic shock, although slightly decreased levels of soluble adhesion molecules were also detectable in patients with chronic heart failure NYHA classes II-III. The signs of systemic inflammation disappeared following successful mechanical circulatory support, but persisted in patients who developed infectious complications. CONCLUSIONS: Our data suggest that a systemic hypoxic and inflammatory syndrome is manifested during end-stage heart failure, such as in patients with sepsis or who have suffered non-infectious insults. During mechanical circulatory support, elevated levels of inflammatory mediators may be indicative of persistent peripheral hypoxia associated with a high risk for infection or sepsis. Therefore, the monitoring of inflammatory mediators should be evaluated as markers of the effectiveness of this therapy.

[Inflammatory mediators in patients with biventricular assist device systems]. / Inflammatorische Mediatoren bei Patienten mit biventrikulären Assist-Device-Systemen.

We studied the plasma levels of TNF-alpha, IL-6, IL-8 and soluble adhesion molecules (sE-Selectin, sL-Selectin, sVCAM-1) immediately before and during mechanical circulatory support with a Biventricular Assist Device System (BVAD-"Berlin Heart") in comparison to patients with chronic heart failure (NYHA classes II/III) and patients with coronary artery disease with normal ventricular function. Additionally, the biocompatibility of the membranes used in the "Berlin Heart" was tested in vitro. IL-6 and IL-8 but not TNF-alpha could only be detected in patients with cardiogenic shock immediately before starting circulatory support. Furthermore, plasma concentrations of soluble adhesion molecules were statistically significantly elevated in patients with cardiogenic shock compared to patients with coronary artery disease. This picture of a systemic inflammatory response syndrome without significant level of TNF-alpha looks quite similar to that seen in patients following trauma and severe operations. During mechanical circulatory support plasma levels of cytokines and soluble adhesion molecules dropped to low levels in patients, who were successfully maintained on BVAD. By contrast, we have found persistently elevated levels of these mediators in patients with fatal outcome. This seems not to be the result of individual distinct response of blood cells to contact with the artificial surfaces of the device. In summary, our data suggest the development of a systemic inflammatory response syndrome may be due to hypoxia during cardiogenic shock. Persistence of systemic inflammation suggests failing of the mechanical support. Therefore, the monitoring of inflammatory mediators may be relevant as a prognostic marker in these patients (disappearance of peripheral hypoxia).

Blood contact with artificial surfaces during BVAD support.

Persistently elevated levels of cytokines (IL-6, IL-8) during the course of mechanical circulatory support correlated well with fatal outcome. To determine the influence of blood/artificial surface interaction on the chronic inflammatory process, we studied the biocompatibility of silicone and polyurethane membranes in vitro. Cultures of isolated mononuclear cells or whole blood were incubated for 24 hours in tubes coated with silicone or polyurethane, both used in the construction of ventricular assist systems. Concentrations of several inflammatory mediators were measured in the supernatant. Our results can be summarized as follows: a) Monocytes were stimulated to release inflammatory cytokines like IL-8 and MIP-1 alpha, particularly when silicone was involved; b) Both silicone and polyurethane stimulated thrombocytes thus resulting in the release of P-Selectin and PDGF-AB, although polyurethane was a stronger stimulus; c) Moderate complement activation was triggered by contact with either of the artificial surfaces. However, the prevention of most of these effects by coating the artificial surface with protein and the lack of correlation between in vitro data and serum levels of IL-6 and IL-8 during the course of circulatory support suggest that the persistence of inflammatory cytokines during BVAD support is not caused by blood/surface interaction.

Interleukin-6 and interleukin-8 concentrations as predictors of outcome in ventricular assist device patients before heart transplantation.

OBJECTIVE: To determine whether the serum concentrations of some circulating cytokines (as highly sensitive markers of inflammation) are of value in predicting the outcome of patients with cardiogenic shock and end-stage heart disease, who undergo ventricular assist device implantation until heart transplantation. DESIGN: Cohort study. SETTING: University teaching hospitals. PATIENTS: Twenty patients with cardiogenic shock or end-stage heart disease were consecutively selected for this study, if assist device implantation was performed as a bridge to heart transplantation. MEASUREMENTS AND MAIN RESULTS: The circulating concentrations of the cytokines interleukin (IL)-1 beta, IL-6, IL-8 and tumor necrosis factor (TNF)-alpha were monitored from the beginning to the end of assist device support two to three times a week, using commercial enzyme-linked immunosorbent assays (ELISA). In all patients, circulating IL-6 and IL-8 values were increased shortly after assist device implantation. In patients with uncomplicated courses, IL-6 and IL-8 concentrations decreased after an initial increase and were low at the time of transplantation, whereas serum cytokine concentrations increased and remained increased in the nonsurvivors (survivors vs. nonsurvivors, p < .001). Circulating IL-1 beta and TNF-alpha concentrations were rarely detectable. CONCLUSIONS: Monitoring of IL-6 and IL-8 values during ventricular assist device support provides a means of early identification of high-risk patients that may allow optimization of antimicrobial therapy and selection of the appropriate time for transplantation.