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Biomedical subjects

C Madl

Publications and source records attributed to C Madl.

At least 19 recordsLinked to original sources

Fulminant lethal tuberculous pneumonia (Sepsis tuberculosis gravissima) with ARDS in a non-immunocompromised western European middle-aged man.

We report the case of a 42 years old, non-immunocompromised native Austrian living in Vienna. He presented at home with severe dyspnea and had to be intubated immediately. Shortly after hospital admission, he developed severe adult respiratory distress syndrome (ARDS) and septic shock with massive, bilobar patchy to confluent infiltrations and a need for norepinephrine. A CT-scan revealed severe loss of functional lung tissue with areas of consolidation and multiple communicating cystic spaces. Air leaking into the mediastinum through fistulas produced pneumomediastinum, pneumoperitoneum, and a massive soft tissue emphysema. Bronchoalveolar lavage performed within the first 24 hours of admission revealed + of acid-fast bacilli. Even though appropriate tuberculostatic medication was started immediately, the patient succumbed the next day to ARDS due to massive tuberculous pneumonia and miliary disease (Sepsis tuberculosis gravissima).

Adult

[Prognostic factors in acute liver failure].

Acute liver failure is defined as acute severe, potentially reversible hepatic failure complicated by cerebral dysfunction. The high mortality rate of between 50% and 90% justifies early transfer to a specialised centre with the possibility of orthotopic liver transplantation to ensure adequate intensive care monitoring and treatment, 57 patients with acute liver failure (34 female, 23 male, aged 6 to 87 years, median 33 years) treated at our intensive care unit during the past 10 years were analysed retrospectively. Various factors and laboratory data were analysed in respect to their prognostic value. Depending on the aetiology, the survival rate in acute liver failure under conservative treatment ranges from 79% (amanita intoxication) to 10% (cryptogenic genesis). The most important predictive parameter is the extent of cerebral dysfunction. The extent of cerebral dysfunction is a determining factor of the survival rate under conservative treatment; it ranges from 94% (patients with hepatic encephalopathy grade I) to 11% (patients with hepatic encephalopathy grade IV). The occurrence of complications such as infections, cerebral oedema, respiratory failure or renal failure is also associated with an unfavourable outcome. Additionally, various laboratory parameters have a predictive ability. The mortality rate of our patients with acute liver failure has decreased from 56% to 32% since early intensive care monitoring and treatment and the possibility of acute orthotopic liver transplantation were established.

Adolescent

[Liver transplantation in acute liver failure].

Acute hepatic failure is characterized by jaundice and hepatic encephalopathy within eight weeks after the onset of disease. Although acute hepatic failure is a rare occurrence, its rapid progression and high mortality (50 to 90%, depending on the etiology of disease) necessitate immediate intervention. In the absence of causal therapy, orthotopic liver transplantation is currently the only definitive and effective means of treating acute hepatic failure in Europe, acute hepatic failure accounts for 11% of all liver transplantations. At the University department of transplantation surgery in Vienna a total of 27 patients with acute hepatic failure underwent 31 liver transplantations in the last 10 years (1.1.1987 to 31.12.1996). Twenty (74%) of the 27 patients survived the acute event and were discharged from hospital in good general condition after a median postoperative stay of 25 days (range 14-81 days). Seven patients (26%) died between the first and 34th postoperative day (median 26 days) in the intensive care unit, although all potential modern options of intensive care and surgery were used. The causes of death were irreversible cerebral edema (n = 3), multiple organ failure due to bacterial sepsis (n = 3) and uncontrollable haemolysis (n = 1). With a 3-year graft survival rate of 70% the 3-year patient survival rate was 74%. A retrospective analysis of our patients revealed that the postoperative graft function and the incidence of re-transplantation were significant prognostic factors (p < 0.05) for survival following orthotopic liver transplantation for acute hepatic failure. In the absence of further prognostically relevant preoperative indices and in consideration of the potentially fulminant progression of disease, we strongly recommend that any patient, in whom acute hepatic failure is suspected, is immediately transferred to a specialized center with experience both in the conservative treatment of acute hepatic failure and emergency liver transplantation.

Adolescent

Previous episodes of hypoglycemic coma are not associated with permanent cognitive brain dysfunction in IDDM patients on intensive insulin treatment.

Intensive insulin treatment of IDDM is associated with increased frequency of hypoglycemic coma. The extent of possible cerebral sequelae after recovery is still unknown. We studied the impact of previous hypoglycemic coma on neurophysiological measures of cognitive brain function in 108 patients with adult-onset IDDM receiving intensive insulin treatment. In the study, 55 IDDM patients (age 38 +/- 14 years, mean +/- SD) who had a history of > or =1 (median 3, range 1-35) comatose hypoglycemic event were compared with 53 IDDM patients (age 34 +/- 12 years) with no history of hypoglycemic events using P300 event-related potentials and psychometric tests (the Mini-Mental State Exam and trailmaking test, part A). Findings on these patients were compared with those from 108 matched healthy control subjects. No difference was observed in P300 latencies and psychometric tests between patients with and without a history of hypoglycemic coma (P300 latency, 346 vs. 342 ms; trailmaking test, 31 vs. 30 s; Mini-Mental State Exam, 29.5 vs. 29.6; NS). In diabetic patients, however, P300 latencies were delayed compared with those of healthy control subjects (344 vs. 332 ms; P < 0.001) and were correlated to diabetes duration but not to total hypoglycemic episodes. Scores on the Mini-Mental State Exam (29.5 vs. 29.6; P = 0.59) and trailmaking test (31 vs. 28 s; P = 0.10) were not different between patients and control subjects. In conclusion, previous episodes of hypoglycemic coma are not associated with permanent impairment of cognitive brain function in patients with adult-onset IDDM receiving intensive insulin treatment compared with patients without such episodes. Cognitive brain function, however, is subclinically impaired in relation to duration of diabetes.

Adult

Detection of subclinical brain dysfunction by sensory evoked potentials in patients with severe diabetic ketoacidosis.

OBJECTIVE: Subclinical brain dysfunction is a potentially deleterious complication of diabetic ketoacidosis but is rarely recognized. Thus, we investigated the diagnostic value of sensory evoked potentials for detecting subclinical brain dysfunction in patients with diabetic ketoacidosis. DESIGN: Prospective trial. SETTING: Intensive care unit in a university hospital. PATIENTS: 5 neurologically asymptomatic patients (Glasgow Coma Scale score 15, slight drowsiness; aged 20 to 66 years) with an established diagnosis of severe diabetic ketoacidosis were studied. MEASUREMENTS AND RESULTS: Short- and long-latency sensory evoked potentials were recorded within 2 h of initiation of therapy for ketoacidosis and 7 days after normalization of ketoacidosis, respectively. Two hours after starting therapy, sensory evoked potential peak latencies were prolonged in all five patients compared to age-matched healthy subjects [cervical N 13 to cortical N 20 interpeak latency of short-latency evoked potentials (mean) 5.8 vs 5.3 ms, p < 0.05; N 35 peak latency 40 vs 34 ms, p < 0.05; N 70 peak latency of long-latency evoked potentials 102 vs 76 ms, p < 0.01]. In all five patients, cervical N 13 to cortical N 20 interpeak latency and N 35 and N 70 peak latency reverted to normal 7 days after recovery from diabetic ketoacidosis. CONCLUSIONS: Our study indicates that the recording of sensory evoked potentials is a sensitive method of detecting subclinical brain dysfunction in patients with severe diabetic ketoacidosis. Since sensory evoked potentials were significantly prolonged in all five patients, this strongly suggests that subclinical brain dysfunction occurs more frequently than is generally recognized.

Adult

Wilson's disease in patients presenting with liver disease: a diagnostic challenge.

BACKGROUND & AIMS: In patients with Wilson's disease presenting with liver involvement, the correct diagnosis is often missed or delayed. The aim of this study was to find an algorithm for diagnosis of this difficult patient group. METHODS: Clinical and laboratory findings of 55 patients with Wilson's disease were evaluated at diagnosis before treatment. Presenting symptom was chronic liver disease in 17 patients, fulminant hepatic failure in 5 patients, hemolysis in 3 patients, and neurological disease in 20 patients, and 10 patients were detected by family screening (siblings). Evaluation included neurological and ophthalmologic examination, routine laboratory tests, and parameters of copper metabolism including liver copper content in 43 liver biopsy specimens. RESULTS: In the whole group, serum ceruloplasmin level was <20 mg/dL in 73%, urinary copper excretion was increased in 88%, and liver copper content was elevated in 91% at diagnosis. Kayser-Fleischer rings were detected in 55%. In contrast to patients with neurological disease (90% Kayser-Fleischer rings, 85% low ceruloplasmin), only 65% of patients presenting with liver disease were diagnosed by these typical findings. Ceruloplasmin levels were lower in patients with Kayser-Fleischer rings or with neurological disturbances than in patients without these symptoms. CONCLUSIONS: The commonly used clinical and laboratory parameters are not sufficient to exclude the diagnosis of Wilson's disease in patients with liver disease of unknown origin.

Adolescent

Sonomorphology of the gallbladder in critically ill patients. Value of a scoring system and follow-up examinations.

PURPOSE: The aim of the study was to assess the value of a scoring system for the diagnosis of acalculous cholecystitis (AC) on ultrasound (US) follow-up examinations and to discuss the merits of scoring system compared to clinical outcome and pathohistologic findings. MATERIAL AND METHODS: In this prospective study, 21 patients at the intensive care unit (ICU) of a medical department were examined by follow-up US. Sonographic parameters of the gallbladder (GB) were obtained (longitudinal and transversal diameter, wall thickening, contents, and pericholecystic fluid) and scored (2 points: distension of GB, thickening of GB wall; 1 point: striated thickening of GB wall, sludge, and pericholecystic fluid; range (0-8). The US findings were correlated with clinical findings and histology at cholecystectomy or autopsy. RESULTS: Of a total of 77 follow-up examinations in these 21 patients, US demonstrated GB distension in 19 patients, wall thickening in 18, sludge in 15, striated thickening of the GB wall in 13, and pericholecystic fluid in 12 patients. Of these, 41 (53%) examinations were scored > or = 6, and 36 (47%) examinations < or = 5. None of the patients with a maximum score during follow-up of < or = 5 (n = 8) had pathohistologic proof of AC or died due to GB complications. Patients with maximum scores of > or = 6: had pathohistologic proof of AC (n = 4); survived with normalization of GB morphology (n = 4); had a normal GB at autopsy (n = 1); or were lost for pathohistologic proof at autopsy (n = 2). CONCLUSION: Our results indicate that regular, short-term follow-up allows early diagnosis and immediate therapy for AC. The scoring system could be helpful in differentiating between patients with an abnormal GB without AC (score < or = 5) and those with an abnormal GB (score > or = 6) with a suspicion of AC. In the latter group, more aggressive diagnostic and therapeutic procedures may be indicated.

Adolescent

Cyclosporine may affect improvement of cognitive brain function after successful cardiac transplantation.

BACKGROUND: The effects of cardiac transplantation on cognitive brain function are uncertain. METHODS AND RESULTS: We measured cognitive brain function and quality of life in out-of-hospital cardiac transplant candidates (n = 55; ejection fraction, 19.9%; age, 54.8 years [means]). After transplantation, the patients were serially reevaluated at 4 months (n = 25) and at 12 months (n = 19). Brain function was measured objectively by cognitive P300 evoked potentials. Additionally, standard psychometric tests (Trail Making Test A, Mini-Mental State Examination, and Profile of Mood State test) were performed. Cognitive P300 evoked potentials were impaired in cardiac transplant candidates (359 ms, recorded at vertex) compared with 55 age- and sex-matched healthy subjects (345 ms, P < .01). Trail Making Test A was also abnormal (45 versus 31 seconds in 55 healthy subjects, P < .01). After transplantation, P300 measures were normalized at 4 months (345 ms, P < .05 versus before transplantation) but declined again at 12 months (352 ms, P = NS versus before transplantation). Stepwise multiple regression analysis revealed that cumulative cyclosporine dosage was the only predictor of individual cognitive brain function 4 months (753 mg/kg body wt, P < .05) and 12 months (2006 mg/kg body wt, P < .01) after transplantation, respectively. CONCLUSIONS: Objective cognitive P300 auditory evoked potential measurements indicate that cognitive brain function is significantly impaired in patients suffering from stable end-stage heart failure. Successful cardiac transplantation is effective to fully normalize impaired brain function. Subsequent relative long-term decline of cognitive brain function after successful cardiac transplantation is strongly suggested to be related to cumulative cyclosporine neurotoxicity.

Affect

Detection of nontraumatic comatose patients with no benefit of intensive care treatment by recording of sensory evoked potentials.

OBJECTIVES: To determine the predictive ability of sensory evoked potential recordings in nontraumatic comatose patients. To evaluate the hypothesis that patients with bilateral absent cortical responses ultimately die despite long-term intensive care treatment. DESIGN: Prospective cohort study. SETTING: Medical intensive care unit (ICU) of a university hospital. PATIENTS: Four hundred forty-one adult nontraumatic comatose patients (unarousable unresponsiveness to external stimulation, Glasgow Coma Score < or = 7) from various causes. Six hundred seventy-six sensory evoked potential measurements were performed within 7 days after onset of coma. MAIN OUTCOME MEASURES: Death or survival to hospital discharge. RESULTS: Eighty-six patients (20%) had a bilateral loss of the cortical evoked potential N20 peak. Despite long-term intensive care treatment, all died without awakening from coma (mortality rate, 100%; 95% confidence interval, 96-100). The mean stay at the ICU after evoked potential measurement until death was 8.1 days (697 patient days). The overall cost of ICU management for these 86 patients accounted for approximately $1,324,300. In the remaining 355 comatose patients with preserved cortical N20 peak, 148 (42%) survived and 207 (58%) died. In this latter group of patients, cervicomedullary N13 to cortical N20 conduction time was prolonged in nonsurvivors (mean +/- SD, 6.7 +/- 1.3 milliseconds) compared with that in survivors (mean +/- SD, 6.4 +/- 1.2 milliseconds, P < .05) and healthy controls (mean +/- SD, 5.5 +/- 0.4 milliseconds, P < .05). Although this difference is statistically significant, a preserved N20 peak is not useful to discriminate whether the individual patient will survive (N13-N20 conduction time of > 7 milliseconds had a positive predictive value of correct prediction of death of 0.67). CONCLUSIONS: Recording of sensory evoked potentials identifies a subgroup of adult nontraumatic comatose patients with a mortality rate of 100% in our sample. In these patients, advanced intensive care treatment should be withdrawn to provide limited ICU resources for patients with higher probability of favorable outcome. We emphasize that these results are not applicable to comatose patients following closed head trauma and particularly not to children.

Adolescent

Outcome prediction for patients with cirrhosis of the liver in a medical ICU: a comparison of the APACHE scores and liver-specific scoringsystems.

OBJECTIVE: To find the most adequate prognostic scoring system for predicting ICU-outcome in patients with decompensated liver cirrhosis in a medical intensive care unit (ICU). DESIGN: Retrospective analysis of patients' records over a 10-year period. SETTING: A medical ICU at the university medical center of Vienna. PATIENTS AND PARTICIPANTS: 94% (n = 198) of all patients with cirrhosis admitted to our medical ICU throughout the 10-year study period. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: From data obtained at admission and at 48 h after admission, scores were calculated using the following scoring systems: Acute Physiology and Chronic Health Evaluation (APACHE) II and III, Scale for Composite Clinical and Laboratory Index Scoring (CCLI), Mayo Risk Score, and Child's Classification. Statistical analysis for the prognostic variables was performed using the chi-square test, t-test, Youden index, and area under a receiver operating characteristic (ROC) curve. APACHE III was found to be the most reliable outcome predictor at admission and after 48 h for patients with decompensated liver cirrhosis (AUC = 0.75 and 0.8, respectively). CONCLUSIONS: To predict the outcome for patients with decompensated cirrhosis of the liver admitted to a medical ICU liver failure alone is not decisive. Liver-specific scoring systems (Mayo Risk Score, CCLI) are adequate, but the APACHE II and III proved to be more powerful, because they include additional physiologic parameters and therefore also take into account additional complications associated with this liver disorder.

APACHE

Beneficial effect of renal transplantation on cognitive brain function.

Cognitive brain dysfunction is a common complication of end-stage renal disease. To investigate the cerebral effect of renal transplantation, we studied P300 event-related potentials--an objective marker of cognitive brain function--trailmaking test and Mini-mental state in 15 chronic hemodialysis patients and 45 matched healthy subjects. Before transplantation, patients showed prolonged P300 latency (364 vs. 337 ms, P < 0.01), smaller amplitude (15.2 vs. 19.1 microV) and scored lower (P < 0.05) in trailmaking test and Mini-mental state as compared to healthy subjects. Following renal transplantation (14 months), P300 latency decreased (337 ms, P < 0.01 vs. before) and amplitude increased (17.4 microV, P < 0.05 vs. before), indicating improved cognitive brain function. The trailmaking test and Mini-mental state tended to improve. Following transplantation, P300 findings, trailmaking test and Mini-mental state were not different from healthy subjects. Additional studies following erythropoietin treatment in 6 of the 15 hemodialysis patients revealed decreased (improved) P300 latency (351 vs. 379 ms before, P < 0.05) with further decrease following transplantation (341 ms, P = 0.06). Our findings indicate that cognitive brain dysfunction in hemodialysis patients may be fully reversed by successful renal transplantation.

Adult

[Acute rhabdomyolysis in status asthmaticus].

Acute rhabdomyolysis is a rare complication in patients with status asthmaticus receiving mechanical ventilation. Individual reports implicate several factors, whereby the simultaneous use of high-dose glucocorticoids and non-depolarizing muscle blocking agents appears to be the major patho-physiological mechanism. A 48 year-old female patient with a 3-year history of granulomatous vasculitis Churg-Strauss was admitted to the intensive care unit (ICU) due to severe status asthmaticus, which necessitated endotracheal intubation and mechanical ventilation. Antiobstructive therapy consisted of beta 2-sympathomimetics, theophylline and high-dose intravenous prednisolone (5440 mg in 10 days). Additionally, the patient was treated with non-depolarizing muscle blocking agents (atracurium 2070 mg over 7 days). Six days after admission to the ICU the patient developed severe rhabdomyolysis, with an increased creatine kinase (CK) level and myoglobinuria. The maximum CK value occurred 12 days after ICU admission (3810 U/l), accompanied by a serum myoglobin level of 13,900 ng/ml. 5 days after cessation of muscle relaxant therapy and reduction of intravenous glucocorticoids, the serum CK level decreased, reaching normal values 9 days later.

Acute Disease

Serial recording of sensory evoked potentials: a noninvasive prognostic indicator in fulminant liver failure.

Sensory evoked potentials are markedly changed in patients with fulminant liver failure. It is unknown, however, whether serial recordings of sensory evoked potentials provide useful prognostic informations for patient management in fulminant liver failure. Ninety recordings of bilateral median nerve-stimulated short- and long-latency sensory evoked potentials were performed in 25 patients with fulminant liver failure (9 patients spontaneously recovered and survived, 8 patients were referred to emergency liver transplantation and 8 patients died). In all nine survivors the cortical long-latency sensory evoked potential N70 peak was constantly detectable between 74 and 162 ms. In all eight patients who subsequently underwent liver transplantation and in seven of eight patients who died, loss of the N70 peak developed during the course of fulminant liver failure. In 4 of 15 patients who were selected for liver transplantation according to the King's College criteria, the N70 peak was constantly detectable. All four transplantation candidates spontaneously recovered and survived without transplantation. In contrast, eight patients never did fulfill the criteria for liver transplantation. Five of them with constantly detectable N70 peak recovered spontaneously. However, in the remaining three patients loss of the N70 peak developed, and they ultimately died. The probability of correct outcome prediction by sensory evoked potentials is superior to that based on clinical criteria alone (0.96 vs. 0.72). Therefore serial recording of sensory evoked potentials may help identify (a) a subgroup among liver transplantation candidates who may spontaneously recover without transplantation and (b) a subgroup of patients with severe brain dysfunction who should undergo early liver transplantation even though they do not fulfill King's College criteria.

Adolescent

Cognitive brain function in non-demented patients with low-grade and high-grade carotid artery stenosis.

Atherosclerotic stenosis of the carotid arteries decreases cerebral flow volume and perfusion, and may result in brain dysfunction. We studied the relationship between the degree of carotid artery stenosis and cognitive brain function in non-demented patients. Cognitive brain function was assessed in 76 patients with carotid artery stenosis (38 patients with low-grade stenosis of 50% or less, and 38 patients with high-grade stenosis of 75% or more) by recording of cognitive P300 auditory evoked potentials and trailmaking test. Results were compared to 70 age-matched healthy subjects. The P300 peak latency was prolonged in patients with high-grade carotid artery stenosis as compared to patients with low-grade stenosis (403 vs. 371 ms, P < 0.01, vertex; 400 vs. 370 ms, P < 0.01, frontal; means). Analysis of variance revealed that the degree of carotid artery stenosis is an independent predictor of prolonged P300 peak latency (P = 0.0001). P300 amplitude (12 vs. 15 microV, vertex; 13 vs. 15 microV, frontal, NS) and trailmaking test (60 vs. 54 s; NS) tended to be worse in the high-grade stenosis group. There was no difference in cognitive brain function between patients with low-grade stenosis and age-matched healthy subjects. Confirmed on sensitive cognitive P300 measurements, we conclude that (a) cognitive brain function is impaired in non-demented patients with high-grade carotid artery stenosis but unaffected in low-grade stenosis; and (b) cognitive brain dysfunction is directly related to the degree of carotid artery stenosis.

Aged