Search PubMed⌕ Search

Biomedical subjects

Ludwig Kramer

Publications and source records attributed to Ludwig Kramer.

16 recordsLinked to original sources
PubMed2005

Relative impact of fatigue and subclinical cognitive brain dysfunction on health-related quality of life in chronic hepatitis C infection.

OBJECTIVES: To assess the relative impact of fatigue and subclinical cognitive brain dysfunction on the impairment of health-related quality of life (HRQL) in hepatitis C virus (HCV) infection. DESIGN AND METHODS: We performed a cross-sectional study in 120 patients with untreated chronic HCV infection to test the hypothesis that the severity of fatigue had an independent effect on HCV-associated impairment of HRQL. Patients were investigated using the short-form-36 questionnaire, the fatigue impact scale, the brief fatigue inventory, and P300 event-related potentials, as an objective correlate of neurocognitive function. Patients with decompensated cirrhosis or clinical depression were excluded. RESULTS: Relative to healthy controls, HCV-infected patients showed significant levels of fatigue (Fatigue Impact Scale, 49 versus 26 points, brief fatigue inventory, 3.0 versus 1.6 points, P < 0.001). Fatigue impact scale and brief fatigue inventory scores were highly correlated (r = 0.77, P < 0.001), demonstrating concurrent validity. Severity of fatigue and age were the only factors independently associated with the impairment of HRQL (P < 0.001). Fatigue was not related to the severity of hepatitis or the degree of subclinical brain dysfunction. CONCLUSION: In untreated patients with chronic HCV infection, fatigue severity and age but not neurocognitive dysfunction or hepatic function are independently associated with impaired HRQL. Both the fatigue impact scale and the brief fatigue inventory are suitable tools to assess the subjective burden of fatigue. Our findings stress the need for effective therapeutic interventions to reduce the burden of fatigue in patients with HCV infection.

Adult↗
PubMed2005

Community-acquired bacteria frequently detected by means of quantitative polymerase chain reaction in nosocomial early-onset ventilator-associated pneumonia.

OBJECTIVE: To test whether real-time polymerase chain reaction allows for rapid quantitative detection of Streptococcus pneumoniae, Chlamydia pneumoniae, Mycoplasma pneumoniae, and Legionella pneumophila in bronchoalveolar lavage fluids and to determine the prevalence of these pathogens in nosocomial ventilator-associated pneumonia. DESIGN: Prospective epidemiologic study applying a new molecular biology-based diagnostic tool during a 27-month period. SETTING: Three medical intensive care units of a tertiary care university hospital. PATIENTS: One hundred patients suffering from nosocomial ventilator-associated pneumonia, hospitalized for > or =14 days, intubated for reasons other than pneumonia, and mechanically ventilated for >48 hrs. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: S. pneumoniae, M. pneumoniae, and C. pneumoniae were detected in bronchoalveolar lavage fluids of 100 patients in 20 (20%), three (3%), and two (2%) cases, respectively. There of 17 (71%) revealed no growth or no significant growth by conventional culture. In one patient, S. pneumoniae and M. pneumoniae were detected simultaneously. Corresponding colony-forming units/mL were partly up to 10 CFU/mL with Gram stainings showing signs of acute inflammation in 80%. A significant temporary correlation between the number of days on ventilator, development of nosocomial pneumonia, and the frequency of detection of these pathogens was found for day 4. CONCLUSIONS: S. pneumoniae, M. pneumoniae, and C. pneumoniae should be considered as causative agents in critically ill patients who develop early-onset nosocomial ventilator-associated pneumonia. Thus, empirical antimicrobial regimens should cover S. pneumoniae, Chlamydia, and Mycoplasma alike. Quantitative polymerase chain reaction is a fast diagnostic tool allowing for detection of these bacteria within 3 hrs in pretreated patients.

Adult↗
PubMed2005

Effects of TIPS on liver perfusion measured by dynamic CT.

OBJECTIVE: Our aim was to measure the arterial, portal venous, and total perfusion of the liver parenchyma with dynamic, single-section CT in patients with liver cirrhosis before and after transjugular intrahepatic portosystemic shunt (TIPS) placement and to compare the results with normal values. SUBJECTS AND METHODS: Perfusion of the liver parenchyma was measured in 24 healthy volunteers and 41 patients with liver cirrhosis using dynamic single-section CT. Seventeen patients underwent TIPS placement, and CT measurements were repeated within 7 days. CT scans were obtained at a single level comprising the liver, spleen, aorta, and portal vein. Scans were obtained over a period of 88 sec (one baseline scan followed by 16 scans every 2 sec and eight scans every 7 sec) beginning with the injection of a contrast agent bolus (40 mL at 10 mL/sec). Parenchymal and vascular contrast enhancement was measured with regions of interest, and time-density curves were obtained. These data were processed with a pharmaco-dynamic fitting program (TopFit), and the arterial and portal venous component and the total perfusion of the hepatic parenchyma were calculated (milliliters of perfusion per minute per 100 mL of tissue). RESULTS: Mean normal values for hepatic arterial, portal venous, and total perfusion were 20, 102, and 122 mL/min per 100 mL, respectively. In patients with cirrhosis before TIPS, mean hepatic arterial, portal venous, and total perfusion was 28, 63, and 91 mL/min per 100 mL, respectively, which was statistically significant for all values (p <0.05). After TIPS, hepatic perfusion increased to a mean value of 48, 65, 113 mL/min per 100 mL for arterial (p <0.01), portal venous, and total (p=0.011) perfusion, respectively. CONCLUSION: In patients with cirrhosis, the hepatic arterial perfusion increased, whereas portal venous and total perfusion decreased compared with that of healthy volunteers. TIPS placement caused a statistically significant increase of the hepatic arterial and total hepatic perfusion. The portal venous parenchymal perfusion remained unchanged.

Adult↗
PubMed2004

Acute liver failure.

Acute liver failure is a rare and life-threatening clinical syndrome following severe hepatic injury. Depending on the rapidity of its development, two distinct complications contribute to a high mortality: in hyperacute liver failure, rapid development of massive hepatic necrosis and apoptosis gives rise to severe hyperammonemia, hepatic encephalopathy and life-threatening cerebral edema. The high risk of cerebral herniation requires early listing for emergency liver transplantation. Patients with hyperacute liver failure surviving the initial episode of cerebral edema have a substantial potential for hepatic recovery. If progressive hepatic failure develops more slowly, astrocytic osmoregulation prevents cerebral herniation in most instances. Unfortunately, these patients have a small potential of hepatic regeneration and transplantation should be performed before renal failure, sepsis or multiorgan failure emerge. Experimental treatment methods including detoxification by artificial or bioartificial liver support or by stimulating hepatic regeneration are currently evaluated. Recognition of ammonia toxicity has stimulated the search for early ammonia-lowering strategies and strongly renewed the interest in dialytic therapies. Anti-apoptotic interventions are among the most promising pharmacological options for the near future.

Brain Edema↗
PubMed2004

Neurocognitive deficit following coronary artery bypass grafting: a prospective study of surgical patients and nonsurgical controls.

BACKGROUND: To objectively measure long-term neurocognitive deficit in patients undergoing coronary artery bypass grafting and compare the findings with nonsurgical controls. METHODS: We prospectively measured neurocognitive function in patients undergoing coronary artery bypass grafting (CABG) with cardiopulmonary bypass (n = 104; mean age 64.1 years old; EuroSCORE 2.7 [means]). A cohort of age- and sex-matched patients (n = 80; mean age 63.4 years old) served as nonsurgical controls. After CABG, neurocognitive function was serially reevaluated at 7-day (n = 104), 4-month (n = 100), and 3-year follow-up (n = 88). Neurocognitive function was objectively measured by means of cognitive P300 evoked potentials. Additionally, standard psychometric tests were performed (Trailmaking Test A, Mini Mental State Examination). RESULTS: As compared to preoperative measures (364 +/- 36 ms), cognitive P300 evoked potentials were prolonged (=impaired) at 7-day (381 +/- 36 ms; p = 0.001), 4-month (378 +/- 31 ms; p = 0.08), and 3-year follow-up (379 +/- 35 ms; p = 0.002), respectively. Trailmaking Test A was abnormal, as compared to preoperative, at 3-year follow-up (p < 0.001). Before the operation, surgical patients were fully comparable in P300 measures to nonsurgical controls (363 +/- 32 ms; p = 0.362). Most importantly, throughout the entire postoperative follow-up cognitive measures in surgical patients were prolonged (=impaired) as compared with controls (7-day p = 0.001; 4-month p = 0.002 and 3-year p = 0.003, respectively). In stepwise multivariate regression analysis, neurocognitive deficit at 4-month follow-up (p < 0.001), age (p = 0.012), and persistent atrial fibrillation (p = 0.024) were predictive for long-term neurocognitive deficit at 3-year follow-up. CONCLUSIONS: As shown by means of objective measures, and in comparison to nonsurgical controls, coronary artery bypass grafting with cardiopulmonary bypass grafting causes long-term neurocognitive deficit.

Aged↗
PubMed2004

Mercury exposure in protein A immunoadsorption.

BACKGROUND: Immunoadsorption is increasingly used to treat antibody-mediated autoimmune diseases. To prevent microbial growth during storage, reusable protein A-Sepharose gel columns are primed with ethyl mercury thiosalicylate (thiomersal, 0.1% solution) and rinsed with phosphate buffer before use. In this study, we tested the hypothesis of systemic mercury exposure in protein A immunoadsorption. METHODS: Whole blood mercury levels were measured by atomic absorption spectroscopy before and after protein A immunoadsorption (11 patients, 26 treatments), anti-IgG immunoadsorption (eight patients, 13 treatments) and LDL apheresis (DALI and Therasorb systems; nine patients, 14 treatments). RESULTS: Patients treated with protein A immunoadsorption had significantly elevated baseline mercury levels compared with the other groups, which were not different from healthy controls. Following protein A immunoadsorption, mercury levels increased from 5.9+/-1.4 microg/l (mean+/-SEM, normal, <5 microg/l) to 32.3+/-5.7 microg/l, P<0.001). In one intensively treated patient, acute neurological toxicity developed at a mercury level of 107 microg/l. Symptoms abated slowly and did not recur after switching to a thiomersal-free system and chelation therapy. No mercury release to patients occurred in anti-IgG immunoadsorption or LDL apheresis treatments. CONCLUSION: This preliminary report suggests that protein A immunoadsorption columns primed with thiomersal during storage may cause a sustained increase of systemic mercury concentrations, which exceed current safety recommendations in a proportion of patients. Considering the potential for mercury-induced toxicity, every effort should be undertaken to reduce systemic mercury exposure, either by adding chelators to the rinsing solution or ideally by replacement of thiomersal.

Adult↗
PubMed2004

Ascites and intraabdominal infection.

PURPOSE OF REVIEW: This review will give an overview of current trends in diagnosis, treatment, and pathogenesis of ascites and intraabdominal infection in cirrhotic and noncirrhotic critically ill patients. RECENT FINDINGS: Single clone-bacterial DNA has been found in sterile ascites and serum, proving the concept of direct translocation. Activation of mesenteric macrophages can be induced by splanchnic vasodilatation but also by hypoxia. Carbon monoxide, an end product of heme catabolism, promotes splanchnic vasodilatation, representing a possible link between gastrointestinal hemorrhage and circulatory dysfunction. Colorimetric test strips and automated counters accurately diagnose spontaneous bacterial peritonitis. Vasopressin V2-antagonists have been introduced as novel therapy for impaired water excretion in hyponatremia. SUMMARY: Emerging pathophysiological concepts have modified the conventional view of hydrostatic and Starling forces in the evolution of ascites. Current data indicate that the dynamic sequence of bacterial translocation, mesenteric inflammation, splanchnic vasodilatation and intrahepatic vasoconstriction determines occurrence, severity, and outcome of ascites and intraabdominal infection.

Ascites↗
PubMed2003

Successful treatment of refractory cerebral oedema in ecstasy/cocaine-induced fulminant hepatic failure using a new high-efficacy liver detoxification device (FPSA-Prometheus).

Ecstasy-induced fulminant hepatic failure is associated with high mortality. If complicated by cerebral oedema, orthotopic liver transplantation is the only established treatment. We report a case of combined ecstasy/cocaine-induced fulminant hepatic failure presenting with severe rhabdomyolysis, myocardial infarction and multiorgan failure. Transplantation was declined by the transplant surgeons because of a history of intravenous drug abuse. As excessive hyperammonaemia (318 mumol/l) and refractory transtentorial herniation developed, treatment with a new liver detoxification device combining high-flux haemodialysis and adsorption (FPSA-Prometheus) was initiated. Within a few hours of treatment, ammonia levels normalised. Cerebral oedema was greatly reduced by day 4 and hepatic function gradually recovered. Following neurologic rehabilitation for ischaemic sequelae of herniation, the patient was discharged from hospital with only minimal deficits. In conclusion, efficient extracorporeal detoxification may be an option for reversal of hyperammonaemia and refractory cerebral oedema in ecstasy/cocaine-induced acute liver failure.

Adult↗
PubMed2003

Neurocognitive deficit following mitral valve surgery.

OBJECTIVE: Neurocognitive deficit is an important complication in patients undergoing open heart surgery. The aim of this prospective, contemporary study was to objectively measure neurocognitive brain function following mechanical mitral valve replacement and mitral valve repair. METHODS: Forty consecutive, unselected patients (mechanical valve replacement n=20, mean age 65+/-14; valve repair n=20, mean age 64+/-7, P=0.896) entered this prospective, contemporary study. Neurocognitive function was objectively measured by means of P300 auditory evoked potentials (peak latencies, ms) and two standard psychometric tests (Mini Mental State Examination, Trailmaking Test A (TTA)), preoperatively, 7 days and 4 months postoperatively. RESULTS: Before operation, neurocognitive brain function was comparable in both patients groups (mechanical valve replacement versus valve repair: P300 potentials 374+/-25 versus 378+/-46 ms; P=0.791 and TTA 57+/-15 versus 54+/-10 s; P=0.552). Following mechanical valve replacement, neurocognitive function continuously worsened (7 day-follow-up: P300 potentials 392+/-28, P=0.001 versus preop and TTA 65+/-17, P=0.0001; 4-month follow-up: P300 potentials 406+/-39, P=0.0004; TTA 69+/-17, P=0.0001). Interestingly, neurocognitive brain function was unaffected in patients undergoing valve repair (7-day follow-up: P300 potentials 386+/-40, P=0.890 versus preop and TTA: 53+/-10, P=0.644; 4-month follow-up: P300 potentials 374+/-36, P=0.166 and TTA 54+/-11, P=0.147). At 4-month follow-up, patients with mechanical prostheses performed worse as compared to valve repair (P300 potentials: P=0.024; TTA P=0.014). CONCLUSION: As shown by P300 auditory evoked potentials and Trailmaking Test A, there is marked neurocognitive damage related to mechanical valve replacement, whereas mitral valve repair does not affect neurocognitive function. This finding supports the beneficial effect of mitral valve repair over mechanical valve replacement in the decision-making tree of borderline cases, which are suitable for both types of procedure.

Adult↗
PubMed2003

Citrate pharmacokinetics and metabolism in cirrhotic and noncirrhotic critically ill patients.

OBJECTIVES: To investigate pharmacokinetics and metabolism of sodium citrate in critically ill patients. To determine the risk of citrate accumulation in the setting of liver dysfunction (cirrhosis, hepatorenal syndrome). DESIGN: Prospective cohort study. SETTING: Intensive Care Unit, Department of Medicine IV, University Hospital Vienna. PATIENTS: Consecutive critically ill cirrhotic (n = 16) and noncirrhotic patients (n = 16). INTERVENTIONS: Infusion of sodium citrate (0.5 mmol.kg-1.hr-1) and calcium chloride (0.17 mmol.kg-1.hr-1) for 2 hrs. Analysis of serial arterial blood samples. MEASUREMENTS AND MAIN RESULTS: Total body clearance of citrate was normal in noncirrhotic critically ill patients but significantly reduced in cirrhotic patients (710 vs. 340 mL/min, p =.008). Citrate peak concentrations and concentration over time were increased by 65% and 114% in cirrhotic patients (p <.001), respectively; volumes of distribution were similar. Net metabolic changes were quantitatively similar, with pH and plasma bicarbonate concentrations increasing more slowly in cirrhotic patients. No citrate-related side effects were noted. Citrate clearance could not be predicted by standard liver function tests and was not appreciably influenced by renal function and Acute Physiology and Chronic Health Evaluation II scores. CONCLUSIONS: This first systematic study on citrate pharmacokinetics and metabolism in critically ill patients confirms a major role of hepatic citrate metabolism by demonstrating reduced citrate clearance in cirrhotic patients. Pharmacokinetic data could provide a basis for the clinical use of citrate anticoagulation in critically ill patients. Provided dose adaptation and monitoring of ionized calcium, citrate anticoagulation seems feasible even in patients with decompensated cirrhosis. Metabolic consequences of citrate infusion were not different between groups in this study but may be more pronounced in prolonged infusion.

APACHE↗
PubMed2002

Cognitive deficit after aortic valve replacement.

BACKGROUND: Impairment of cognitive brain function after coronary artery bypass grafting (CABG) is well known. In contrast the potential neurocognitive damage related to aortic valve replacement (AVR) is uncertain. METHODS: In this contemporary case-matched control study we followed 30 patients (mean age 70 years) receiving isolated AVR with a biological prosthesis. A cohort of sex-and age-matched patients (n = 30, mean age 70 years) receiving CABG with cardiopulmonary bypass served as controls. Cognitive brain function was measured by means of auditory evoked P300 potentials (peak latencies, ms) before the operation and 7 days and 4 months after the operation. Additionally, two standard psychometric tests (Mini-Mental State Examination and the Trailmaking Test A) were performed. RESULTS: In preoperative measures there was no difference between patients undergoing AVR and patients undergoing CABG (AVR 378 +/- 37 ms, CABG 374 +/- 32 ms, p = 0.629). One week after surgery P300 peak latencies were prolonged (impaired) in both groups compared with preoperative values (AVR 405 +/- 43 ms, p = 0.001; CABG 398 +/- 44 ms, p = 0.004). At this point of follow-up there was no difference between the groups (p = 0.607). Finally, 4 months after surgery P300 auditory evoked potentials returned to normal in the CABG group (380 +/- 24 ms, p = 0.940) while in contrast in the valve group they continued to become prolonged (worsened) compared with preoperative values (410 +/- 47 ms, p = 0.005). At this time of follow-up P300 peak latencies were prolonged in AVR patients as compared with CABG patients (p = 0.032). The Trailmaking Test A and Mini-Mental State Examination failed to discriminate any difference. CONCLUSIONS: Four-month impairment of cognitive brain function is more pronounced in patients undergoing biological AVR as compared with age-matched control patients undergoing CABG. Further studies are needed to clarify the potential pathologic mechanisms causing an ongoing cognitive impairment in patients with biological aortic valve prostheses.

Aged↗
PubMed2002

Subclinical impairment of brain function in chronic hepatitis C infection.

BACKGROUND/AIMS: Central nervous system abnormalities such as fatigue and depression occur more frequently in chronic hepatitis C virus (HCV) infection than in many other causes of chronic liver disease. The finding that fatigue is unrelated to activity of hepatitis or mode of infection could indicate an independent effect of HCV on brain function. This study tested the hypothesis of a subclinical cognitive dysfunction in HCV-infected patients. METHODS: One-hundred untreated HCV-RNA positive biopsy-proven patients were investigated by P300 event-related potentials, a sensitive electrophysiologic test of cognitive processing. Health-related quality of life and fatigue were assessed using the SF-36 questionnaire and the Fatigue Impact Scale, respectively. RESULTS: Cognitive brain function was subclinically impaired in the cohort of HCV-infected patients as indicated by significantly prolonged P300 latencies (P=0.01 for comparison to matched healthy subjects) and reduced P300 amplitudes (P<0.001, respectively). Seventeen of the 100 HCV-infected patients had P300 latencies outside the age-adjusted normal range. Abnormal P300 characteristics were not related to the degree of histologic or biochemical activity of hepatitis, severity of fatigue or mental health impairment. CONCLUSIONS: This study demonstrates that patients with HCV infection showed a slight but significant neurocognitive impairment, possibly indicating a further extrahepatic manifestation of chronic hepatitis C.

Adult↗
PubMed2002

Impaired subcortical and cortical sensory evoked potential pathways in septic patients.

OBJECTIVE: Sensory evoked potential (SEP) peak latencies were recorded in order to evaluate the incidence and severity of septic encephalopathy, testing the hypothesis that the occurrence of septic encephalopathy is more frequent than generally assumed. DESIGN: Prospective cohort study. SETTING: Medical intensive care unit of a university hospital. PATIENTS: Sixty-eight critically ill patients were studied within 48 hrs after the development of severe sepsis (n = 41) or septic shock (n = 27). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Septic encephalopathy was defined as prolongation of SEP peak latencies beyond the upper limit of the reference range of subcortical (N13-N20 interpeak latency) and cortical SEP pathways (N20-N70 interpeak latency), as well as asymmetry of peak latencies marked by the presence of subclinical cerebral focal signs. Subcortical SEP pathways were impaired in 34% and cortical SEP pathways in 84% of all patients. The prolongation of the cortical SEP pathway correlated with the Acute Physiology and Chronic Health Evaluation III score (r = 0.23; p <.0001). SEP peak latencies did not differ in patients with severe sepsis compared with those with septic shock. Subclinical cerebral focal signs were present in 24% of the subcortical SEP pathways and in 6% of the cortical SEP pathways. CONCLUSIONS: Septic encephalopathy occurs more frequently than generally assumed, and its severity is associated with the severity of illness. The impairment of subcortical and cortical SEP pathways was not different between patients with severe sepsis and those with septic shock.

Brain Diseases↗
PubMed2002

Neurophysiological evidence of cognitive impairment in patients without hepatic encephalopathy after transjugular intrahepatic portosystemic shunts.

OBJECTIVES: We aimed to test the hypothesis that subclinical cognitive brain dysfunction in cirrhotic patients would deteriorate after a transjugular intrahepatic portosystemic shunt (TIPS) in the absence of clinically detectable hepatic encephalopathy. METHODS: Out of 49 consecutive cirrhotic patients receiving elective TIPS for recurrent variceal hemorrhage, we identified 22 patients who were not encephalopathic and had not undergone liver transplantation at 6-month follow-up and confirmed TIPS patency by Doppler ultrasound. Patients were tested before and 6 months after TIPS implantation using event-related (P300) cognitive evoked potentials, late somatosensory median nerve (N70) potentials, and standard psychometric tests (Mini-Mental State and trailmaking test A). Twenty-two age-matched healthy subjects served as controls. RESULTS: Relative to controls, patients showed significantly impaired P300 and N70 latencies and abnormal psychometric test results at baseline. Six months after the TIPS, a further impairment of P300 latency was observed (p = 0.005), whereas no relevant changes in N70 latency and psychometric test results occurred. CONCLUSIONS: In cirrhotic patients with portal hypertension, neurophysiological signs of cognitive brain dysfunction are detectable in the absence of hepatic encephalopathy. A further subclinical deterioration of cognitive processing was observed 6 months after the TIPS. These findings demonstrate an aggravation of subclinical hepatic encephalopathy after a TIPS.

Adult↗
PubMed2002

Hepatorenal syndrome.

The hepatorenal syndrome is defined as functional renal failure in advanced chronic or acute liver disease with portal hypertension. Morphologic abnormalities of the kidneys are frequently absent and tubular function is preserved. Patients with the hepatorenal syndrome are characterized by progressive splanchnic and systemic vasodilation and decreased effective arterial blood volume. Compensatory activation of vasoconstrictory systems maintains systemic hemodynamic stability but causes progressive afferent renal vasoconstriction, leading to reduction of glomerular filtration rate. Renal failure may be rapidly progressive (type I hepatorenal syndrome, frequently associated with spontaneous bacterial peritonitis) or may develop more slowly (type II). Orthotopic liver transplantation is the best current treatment and leads to a gradual recovery of renal function in the vast majority of patients. Because mortality of type I hepatorenal syndrome is excessive, supportive treatment by vasoconstrictor drugs, transjugular intrahepatic portosystemic shunt, and renal replacement therapy has been investigated to achieve stability until transplantation. The definite role of these promising developments, however, is still uncertain, emphasizing the need for large prospective multicentric investigations.

Ascites↗