Rudolf Hess - The Doppelgänger conspiracy theory disproved.

The Deputy Führer of the Third Reich Rudolf Hess was captured after a controversial flight to Scotland in 1941. Hess was sentenced to life imprisonment during the Nuremberg War Crimes Trials. He was detained in Berlin's Spandau Prison under the official security designation 'Spandau #7.' Early doubts arose about the true identity of prisoner 'Spandau #7.' This evolved to a frequently espoused conspiracy theory that prisoner 'Spandau #7' was an imposter and not Rudolf Hess. After Hess's reputed 1987 suicide, the family grave became a Neo-Nazi pilgrimage site. In 2011, the grave was abandoned and the family remains cremated. Here we report the forensic DNA analysis of the only known extant DNA sample from prisoner 'Spandau #7' and a match to the Hess male line, thereby refuting the Doppelgänger Theory.

[Alleged assault in a forest: An unusual case of self-inflicted blunt injury]. / Angeblicher Überfall im Wald--ein ungewöhnlicher Fall von Selbstverletzung durch stumpfe Gewalt.

The medico-legal assessment of potentially self-inflicted injuries is an important field of clinical forensic medicine. Compared with sharp force injuries, it is much more difficult to distinguish blunt injuries caused by another party from self-inflicted lesions. We present a case of a young female doctor, who was allegedly attacked by an unknown stranger during her evening walk in the woods. She claimed to have been hit repeatedly on the head and arms with a stone. During the forensic investigation, blunt injuries could be confirmed on her head and forearms. Based on the arrangement and intensity of the injuries, together with the result of a bloodstain pattern analysis of the weapon, the victim's statement could be disproved. After being confronted with the results of the investigation, the woman admitted to have inflicted the injuries herself. This case is an unusual and rare example of self-inflicted blunt injury. It shows that the criteria of self-inflicted injuries can also be applied to blunt trauma. However, due to the small number of cases, a high degree of caution is required from the forensic expert.

Another phantom from the morgue--a case of instrument-born sample contamination in the course of identifying an unknown deceased.

Due to its high reliability, DNA-typing is the method of preference in the field of osseous human remains identification. Nevertheless, contaminations from various sources have been shown to be inherent to the system, especially if the DNA-yield of samples under investigation is expected to be at a low level. For this reason a special focus has to be put on sampling procedures and contamination control in order to prevent from false results. In this study we present an illustrative case report followed by particular recommendations for taking samples from osseous human remains.

Driving under the influence of drugs and alcohol in Salzburg and Upper Austria during the years 2003-2007.

Until 2002 in Austria a blood sample could not be drawn due to regulations stipulated by the Austrian constitution. During the years 2003-2007 alcohol, pharmaceuticals and illicit drugs were analyzed in 1167 blood samples from cases of suspected and drugged drivers. In accordance with the findings of the EU-project Rosita, a wide variety of illicit drugs and medications could be found in blood samples of the drivers where cannabis (50%), opiates (20%), amphetamines (18%), cocaine (15%) and benzodiazepines (20%) were those with the highest prevalence. To enable police and medical officers to identify drivers under the influence of cannabis, a newly developed urinary road-site-test system, Check 24 (Protzek GmbH, Germany), with two different cut-off values for THCCOOH-glucuronide was used. So far, it was not possible to draw any conclusions from a cannabinoid positive urine sample to the actual influence of a driver due to the previous consumption of cannabis. Using this test a better differentiation between recent and temporal earlier consumption was possible. In addition to using the Check 24 system the technology of pupillography (AMTech GmbH, Germany) was applied in cases of drugged driving. For the first time the authors were able to predict the presence of at least one central nervous active substance in the blood of a drugged driver.

Pupil function as a parameter for assessing impairment of the central nervous system from a traffic-medicine perspective.

To evaluate an individuals driving safety objective measurement methods are required which allow reproducible, reliable and subsequently verifiable data to be collected. In this study, we exposed healthy test subjects (n=41), as well as persons who were under the influence of drugs and/or medication (n=105), to different light stimuli and tested the pupillary light reflex in order to gain a better understanding of the physiological and pathological pupil function. The tests were performed using a "Compact Integrated Pupillograph" (CIP), which enables pupil reactions to be measured using infrared technology. The primary aim was to assess the applicability and value of infrared pupillography as an objective measurement method for assessing persons with impairments of the central nervous system in terms of their driving safety and fitness to drive. There were highly significant differences for almost all the evaluated parameters between the groups tested. In particular, the synoptic examination of numerous parameters measured by this system, and the possibility of examination under various conditions, especially in terms of light stimuli intensity, made it possible to achieve highly significant differentiation between persons with impairments of the central nervous system and control persons. On the basis of the results obtained, it can be categorically stated that infrared pupillography represents an objective method of measuring pupil function. In order to increase legal certainty it would thus appear desirable to make infrared pupillography a routine part of police checks.

Invasive fungal infections and (1,3)-beta-D-glucan serum concentrations in long-term intensive care patients.

OBJECTIVE: Invasive fungal infections are associated with high morbidity and increased mortality. This study was performed to assess the epidemiology of fungal infections and to determine (1,3)-beta-D-glucan serum concentrations in patients admitted to intensive care units (ICUs). PATIENTS AND METHODS: Overall 197 patients were admitted to nine medical and surgical intensive care units (ICUs) at a 2200-bed university hospital during a 3-month period. Retrospectively, the patients were split into three groups: group A comprised 24 patients with proven invasive fungal infections admitted for a median of 40 days. Group B comprised 58 patients who were admitted to the ICU for 30 days but without fungal infection. One hundred and fifteen post-operative patients served as controls (group C). The levels of (1,3)-beta-D-glucan were monitored in all patients twice weekly during their ICU admittance. RESULTS: Average (1,3)-beta-D-glucan concentrations were significantly higher in the patients with fungal infections compared to group B and group C (median 44 vs. 22 and 12.9 pg/ml, respectively; p<0.001). For a serum (1,3)-beta-D-glucan level of 40 pg/ml, the sensitivity, the specificity, the positive predictive value, the negative predictive value, the area under the curve of the receiver operating characteristics (AUC ROC) curve, the likelihood ratio (LR)+ and LR- were 52.2, 75.9, 46.2, 80, 0.7, 2.16, and 0.63, respectively, on day 7. Patients in group A had bacterial infections significantly more often than patients in group B (p=0.003). The hospitalization before ICU admittance for group A was significantly longer than for groups B and C (median 19 (group A) vs. 6 (group B) vs. 10 (group C) days; p<0.05). CONCLUSIONS: Longer hospitalization and multiple bacterial infections were found to be the main risk factors for invasive fungal infections. Long-term ICU patients have elevated (1,3)-beta-D-glucan levels, not only due to invasive fungal infections, but also due to the serious underlying diseases and conditions, inter-current complications, and intensive care measures. Yet, persistently high serum levels of (1,3)-beta-D-glucan in ICU patients may be indicative of invasive fungal infections and warrant additional diagnostic efforts.

Application of ion mobility spectrometry in cases of forensic interest.

Ion mobility spectrometry (IMS) has been known as an analytical technique since the late 1960s and early 1970s. To date, it has been successfully utilized for the detection of environmental pollutants, warfare agents, explosives, herbicides, pesticides, petroleum products as well as for the detection of prescription and illicit drugs. In this paper the authors describe the use of the IMS technology in cases of forensic interest in Salzburg, Austria. We report the use of the IMS methodology for the rapid analysis of hallucinogenic mushroom material as well as for the analysis of samples taken after an explosion. A new application of the IMS technology for the analysis of postmortem sweat samples for drugs is also presented.

A woman with red eyes and hypokalemia: a case of acquired Gitelman syndrome.

Gitelman syndrome is a rare hereditary disorder of the thiazide-sensitive NaCl transporter in the distal renal tubular cells, but mimicking of such hereditary tubular disorders has been described in different autoimmune diseases (Sjögren syndrome, SLE, ...). A 62-year-old woman with painful red eyes and sicca syndrome presented at the ophthalmological department. The diagnostic evaluation identified a Sjögren syndrome with early endophthalmitis as the reason for the red eyes. Results of laboratory examination indicated severe hypokalemia, metabolic alkalosis and hypomagnesemia, although this had not been seen years earlier. Together with the urine analysis, a rare case of an acquired Gitelman syndrome was diagnosed. Substitution with potassium and magnesium improved the initial symptoms of weakness, but renal electrolyte wasting persisted even after treatment of Sjögren syndrome. In patients with autoimmune disease, laboratory analysis of serum electrolytes should be performed because different acquired tubular disorders can lead to severe hypokalemia.

Treatment of adult patients with sepsis-induced coagulopathy and purpura fulminans using a plasma-derived protein C concentrate (Ceprotin).

BACKGROUND AND OBJECTIVES: The aim of this study was to document the effects of supplementation with a plasma-derived protein C concentrate in adult patients with infectious purpura fulminans. MATERIALS AND METHODS: We report the effect of the administration of a human protein C concentrate (Ceprotin, Baxter, Vienna, Austria) in eight adult patients with purpura fulminans. Five patients received the concentrate as level-adjusted continuous infusion (10 U/kg/h, target protein C activity 100%) and three patients received the concentrate as bolus infusions (100 U/kg every 6 h) in addition to standard sepsis therapy. Heparin, fresh-frozen plasma, antithrombin- and fibrinogen concentrates, low-dose rtPA, and platelet transfusions were given when appropriate. RESULTS: Six patients had overt disseminated intravascular coagulation: platelets, 19 g/l; fibrinogen, 60 mg/dl; antithrombin, 47%; prothrombin time, 32%; activated partial thromboplastin time (APTT), 88 s; d-dimer, 66 microg/ml; protein C activity, 29% (medians). Five patients had septic shock, six renal failure and four respiratory failure. Patients received between 5000 and 77,000 U of protein C concentrate over 2.5 days (median); the protein C activity increased to 184% (median) and coagulopathy resolved within 3 days in seven of the eight patients. Six patients survived, one died early from fulminant sepsis, and one died after 14 days from candida sepsis. CONCLUSIONS: Our data suggest that treatment with a plasma-derived protein C zymogen concentrate might be a useful support in adult patients with purpura fulminans.

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.

Citrate kinetics in patients receiving long-term hemodialysis therapy.

BACKGROUND: Regional anticoagulation using sodium citrate is used increasingly in hemodialysis patients at high risk for bleeding. However, citrate metabolism has never been evaluated systematically in hemodialysis patients, and it remains to be shown that citrate is cleared adequately in the presence of renal dysfunction. This study compares the pharmacokinetics of citrate in hemodialysis patients with minimal residual function with that in patients with normal renal function. METHODS: Long-term hemodialysis patients (n = 7) and patients without renal failure (n = 11) were investigated during routine immunoadsorption treatment by using a standardized citrate infusion protocol. Serial analysis of blood samples was performed before, during, and up to 120 minutes after citrate infusion (0.33 mmol/kg/h). Citrate plasma concentrations were measured colorimetrically. In addition, ionized calcium, pH, and bicarbonate were measured by using a blood gas analyzer. RESULTS: Basal (0.09 +/- 0.03 versus 0.12 +/- 0.03 mmol/L; P = not significant) and peak citrate concentrations were similar in both groups (1.24 +/- 0.42 versus 1.19 +/- 0.33 mmol/L; P = not significant). Citrate clearance was similar in patients with renal failure (0.31 +/- 0.06 L/min) and controls (0.35 +/- 0.11 L/min; P = 0.47). Effects on pH were minimal and did not differ between groups. No patient developed complications from citrate infusion. CONCLUSION: Compared with controls, citrate clearance and metabolism in long-term hemodialysis patients is not impaired, and no significant acid-base disorder occurred during citrate anticoagulation. From these data, it is tempting to conclude that citrate anticoagulation can be used safely in patients with chronic renal failure on regular hemodialysis therapy.

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.

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.

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.

Neurocognitive deficit following aortic valve replacement with biological/mechanical prosthesis.

OBJECTIVE: The aim of this study was to objectively measure neurocognitive deficit following aortic valve replacement with a mechanical or biological prosthesis. MATERIALS AND METHODS: In this prospective, contemporary study we followed 82 consecutive patients undergoing isolated aortic valve replacement with either a mechanical (n=29, mean age=52+/-7 years) or a biological (n=53, mean age=68+/-10 years) valve prosthesis. Neurocognitive function was measured by means of objective P300 auditory evoked potentials (peak latencies, ms) and two standard psychometric tests (Trailmaking Test A, Mini Mental State Examination) before the operation, 7 days and 4 months after the operation, respectively. RESULTS: Since P300 peak latencies increase with age, preoperative P300 measures are lower in patients receiving mechanical valves (360+/-35 ms, mean 52 years) as compared to patients receiving biological valves (381+/-34 ms, 68 years, P=0.0001). Seven days after surgery, P300 peak latencies were prolonged (-worsened) in both groups as compared to preoperative values (mechanical valves: 384+/-36 ms; P=0.0001 and biological valves: 409+/-39 ms; P=0.0001). Although on a different level (-age-related), this development was comparable within both groups (P=0.800). Four months after surgery, P300 peak latencies normalized in the mechanical valve group (372+/-27 ms, P=0.857 versus preoperative), while in contrast in the biological valve group they remained prolonged (417+/-37 ms, P=0.0001). We found no difference within patients receiving different types of biological or mechanical aortic valves. CONCLUSION: Postoperative neurocognitive damage is not reversible in (-elderly) patients with biological aortic valve replacement, while in contrast postoperative neurocognitive damage is reversible in (-younger) patients with mechanical valve replacement. For this contrary development, age seems to be most important, whereas damage related to type of valve prosthesis may be overestimated.

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.

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.

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.