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M Mauer

Publications and source records attributed to M Mauer.

At least 37 records · Page 2Linked to original sources

Heterogeneous nature of microalbuminuria in NIDDM: studies of endothelial function and renal structure.

Microalbuminuria (MA) is associated with microangiopathy (renal and retinal lesions) in insulin-dependent diabetic (IDDM) patients. In contrast MA does not reflect microvascular damage in a substantial number of non-insulin-dependent diabetic (NIDDM) patients. MA predicts cardiovascular disease in NIDDM patients with increased von Willebrand factor (vWF) plasma levels which are hypothesized to reflect endothelial dysfunction. However, it is not known whether MA is consequent to generalised endothelial dysfunction or to renal injury. Thus, this study evaluated vWF plasma levels in relation to renal and retinal structural abnormalities in NIDDM patients with MA. Kidney biopsies, fundoscopy and measures of vWF plasma levels were performed in 32 NIDDM patients with MA. These patients were allocated to two renal structural categories: A) Without renal structural abnormalities (C I, n = 10): normal or near-normal renal structure, and B) With renal structural abnormalities (n = 22), further divided into: C II (n = 12) with typical diabetic nephropathology, predominantly glomerulopathy, and C III (n = 10) with atypical patterns of renal injury (more advanced tubulo-interstitial and arteriolar than glomerular changes). vWF plasma levels were significantly higher in category B (C II: 195+/-49% and C III: 161+/-46%) than in category A (C I: 119+/-42%), (chi-square, p < 0.05). Diabetic retinopathy was also related to vWF plasma levels (ANOVA, p < 0.05). These data suggest that there are two types of MA in NIDDM: one associated with increased vWF levels, established renal injury and frequently retinopathy, and the other characterized by normal vWF levels, normal renal structure and absent or mild diabetic retinopathy. We propose that vWF plasma levels in NIDDM patients with MA may help to identify patients with important renal structural changes, increased retinopathy risk and, perhaps, generalised endothelial dysfunction. Whether vWF plasma levels predict end-stage renal disease and cardiovascular events deserves longitudinal studies.

Adult↗

Chronology of renal scarring in males with Alport syndrome.

We investigated the onset of renal scarring in 62 males (aged 4-26 years) with Alport syndrome by measuring cortical interstitial volume fraction [Vv (interstitium/cortex)] and percentage global glomerular sclerosis in kidney biopsies. Male pediatric (n = 9) and adult (n = 7) donor kidneys served as controls. Creatinine clearance at the time of biopsy was available for 43 Alport patients. A statistically insignificant correlation between age and Vv (interstitium/cortex) was observed in normal subjects (r = +0.47, slope = 0.0009, P = 0.07). In the Alport patients, age was significantly correlated with Vv (interstitium/cortex (r = +0.49, slope = 0.01, P = 0.001) and global glomerular sclerosis (r = +0.41, P = 0.01), and inversely correlated with creatinine clearance (r = -0.33, P = 0.04). Creatinine clearance was inversely correlated with Vv (interstitium/cortex) (r = -0.78, P = 0.001) and global glomerular sclerosis (r = -0.74, P = 0.001). The correlation with creatinine clearance was especially strong for Vv (interstitium/cortex) values above the normal range, i.e., > 0.2 (r = -0.82, P = 0.001), and was absent for Vv (interstitium/cortex) < 0.2 (r = -0.119, P = 0.55). Creatinine clearance values less than 80 ml/min per 1.73 m2 occurred more frequently in patients with Vv (interstitium/cortex) values > 0.2 (P < 0.0001) and in patients with > 10% globally sclerosed glomeruli (P < 0.001). Patients < or = or > 10 years of age differed in Vv (interstitium/cortex) [0.13 +/- 0.09 (mean +/- SD) vs. 0.24 +/- 0.026, P < 0.001], the frequency of Vv (interstitium/cortex) > 0.2 (3/32 vs. 15/31, P < 0.0001), the frequency of > 10% globally sclerosed glomeruli (3/33 vs. 11/30, P < 0.05), mean creatinine clearance (113 +/- 7 vs. 84 +/- 10 ml/min per 1.73 m2, P = 0.057), and the frequency of creatinine clearance < 80 ml/min per 1.73 m2 (1/20 vs. 11/23, P < 0.01). Thus, reduced creatinine clearance in males with Alport syndrome is associated with Vv (interstitium/cortex) > 0.2 and > 10% globally sclerosed glomeruli. These are frequently detectable in the 2nd decade. We hypothesize that most Alport males will require intervention during the 1st decade for optimal preservation of kidney function.

Adolescent↗

Hemodialysis catheter placement and recirculation in treatment of hyperammonemia.

A 2-year-old girl with carbamoyl phosphate synthetase deficiency underwent emergency hemodialysis (HD) for treatment of acute life-threatening hyperammonemia. HD was performed via catheters placed in each femoral vein serving as vascular access. The tip of one of the catheters (aspirating line) was in the left external iliac vein and the tip of the other catheter (the return line) was in the inferior vena cava (IVC). High blood flow rates were used in order to rapidly lower the blood ammonia (NH3) levels. However, unanticipated marked recirculation in the IVC, between the dialysis aspirating and return catheters, was encountered, preventing significant reduction in blood NH3. The recognition of this problem, suggested solutions, and prevention are described.

Ammonia↗

Proximal tubular basement membrane width in insulin-dependent diabetes mellitus.

Although glomerular structure has been studied, careful evaluation of tubular basement membrane (TBM) structure in diabetes in humans has not been done. We measured proximal TBM width, glomerular basement membrane (GBM) width, mesangial fractional volume [Vv(Mes/glom)], mesangial matrix fractional volume [Vv(MM/glom)], and cortical interstitial fractional volume [Vv(Int/cortex)] in 35 insulin-dependent diabetic (IDDM) patients and 20 controls. The patients' mean age was 28 +/- 10 years (X +/- SD) and IDDM duration was 17 +/- 8 years. Twenty-five patients were normoalbuminuric, four microalbuminuric, and six had overt proteinuria. Tubular basement membrane and GBM widths were measured by the orthogonal intercept method and mesangial and interstitial parameters by point counting. The TBM width was 915 +/- 320 nm in IDDM patients and 558 +/- 116 nm in controls (P = 0.0005); the TBM width was also increased in normoalbuminuric patients (849 +/- 297 nm, P = 0.0005). The TBM width was strongly directly related to GBM width (r = 0.67, P < 0.001), Vv(Mes/glom) (r = 0.52, P < 0.01), and Vv(MM/glom) (r = 0.61, P < 0.001), but only weakly to Vv(Int/cortex) (r = 0.29, NS). The TBM width (r = 0.65, P < 0.001) and GBM width (r = 0.65, P < 0.001) were strongly related to hemoglobin A1C (HbA1C), while the Vv(Mes/glom) (r = 0.35, P < 0.05) and Vv(Int/cortex) (r = 0.30, NS) were only weakly related to HbA1C. Thus, increased proximal TBM width is an integral component of early nephropathology in IDDM patients. This study suggests that the metabolic disturbances of diabetes are strong determinants of the constellation of structural abnormalities occurring in human diabetic nephropathy.

Adolescent↗

Relationships of cell proliferation and expression of integrin subunits and type I collagen in skin fibroblasts with renal lesions in patients with IDDM.

Previous studies have shown that cultured skin fibroblasts (SFs) from insulin-dependent diabetic mellitus (IDDM) patients with diabetic nephropathy (DN) exhibit both increased proliferation and Na+/H+ antiporter activity. The present study correlated the growth rate and mRNA expression of integrin subunits, extracellular matrix molecules, and transforming growth factor-beta in cultured SFs, with the biopsy determined rate of development of DN lesions ranging from slow to rapid in nine IDDM patients. These varying rates of development of DN lesions were expressed by a mesangial expansion score as estimated by the rate of change in mesangial fraction volume per year. Cultured SF proliferation by direct cell counts positively correlated with mesangial expansion score (r = 0.65; P < 0.05). Expression of cultured SF alpha3 integrin subunit mRNA levels, as well as type I collagen mRNA (P < 0.05 for both), but not transforming growth factor-beta mRNA levels (Northern blot analysis), were also positively correlated with mesangial expansion score. We postulate that these observations of correlations between activities of cultured SFs and the rate of progression of DN lesions may be predictive of the risk to develop clinical DN in IDDM, may be in part genetically regulated, and may be of pathogenetic importance.

Adult↗

[Active compression-decompression resuscitation. Improved survival rate in an emergency medicine system with emergency physician assistance?].

BACKGROUND: Improved cardiopulmonary circulation with active compression-decompression resuscitation (ACD-CPR) has been demonstrated in studies using different animal models and a small number of human in cardiac arrest (CA). However, prehospital studies have shown both positive and no extra benefit of ACD-CPR on survival rates and neurologic outcome. MATERIAL AND METHODS: The aim of our prospective study was to compare standard manual CPR (S-CPR) to ACD-CPR as the initial technique of resuscitating patients with out-of-hospital CA with respect to survival rates and neurological outcome in our two-tiered EMS system with physicians in the field. RESULTS: Patients with out-of-hospital CA treated by emergency medical services (EMS) personnel were randomly assigned to 1 of 2 groups (ACD-CPR versus S-CPR). The treatment groups were similar with respect to age, sex, time interval from collapse to CPR, defibrillation and first epinephrine medication. There was no difference between the ACD group and the standard CPR group in terms of survival rates and neurologic outcome. No differences occurred concerning complications of CPR. CONCLUSION: In our two-tiered EMS system with physician-staffed ambulances ACD-CPR neither improved nor impaired the survival rates and the neurological prognosis in patients with out-of-hospital cardiac arrest. Our results are in accordance with other studies carried out in EMS systems, with first tier call-response intervals between 4 and 6 min.

Adult↗

Delayed acute renal failure in post-transplant period in young children from unexplained etiology.

This report describes six young children (5 male) who developed delayed acute renal failure (DARF) in the early post-kidney-transplant (Tx) period in the absence of acute rejection (AR) or other diagnosable conditions. These young children, aged 16.5 +/- 3.1 (12-21) months [mean +/- SD, (range)] and weighing 8.5 +/- 1.7 (7.1-11.4) kg received a primary renal Tx (5 living-related donor, 1 cadaver) between 1984 and 1992. Immunosuppression included prednisone, azathioprine, and Minnesota antilymphocyte globulin (MALG, n = 5); one patient received cyclosporine and no MALG. Initially, all patients had good urine output (UO). They became systemically ill and abruptly developed diminished UO on post-operative day (POD) 6.5 +/- 1 (4-8). DARF was accompanied by fever (39.1-40.4 degrees C, n = 6), thrombocytopenia (platelets < 100,000/mm3, n = 6), leukocytosis, or leukopenia (white cell count > 20,000/mm3, n = 4 or < 1,000/mm3, n = 1). Four patients had diarrhea. Three had ascites and one was surgically explored for suspected urinary leak. None showed significant urinary obstruction by renal ultrasound. Renograms showed intact blood flow. Renal biopsy showed tubular ectasia (n = 6), vascular congestion (n = 5), focal glomerular endothelial swelling (n = 4), and capillary thrombi (n = 3). None showed AR. Five patients required dialysis for 11 +/- 4 (7-15) days. All patients survived. One patient, treated for suspected AR with the monoclonal antibody OKT3, developed shock and lost her graft on POD 12 due to vascular thrombosis. Renal functional recovery in the remaining five patients took 14 +/- 5 (6-20) days and their serum creatinine at discharge was 0.7 +/- 0.5 (0.3-1.6) mg/dl. We report DARF from undetermined etiology occurring in the first 2 weeks of renal Tx in young children. Treatment is supportive care including dialysis. Recognition of this complication will help avoid risky investigations or unnecessary treatment for rejection.

Acute Kidney Injury↗

Modified Method for Competitive Reverse Transcription Polymerase Chain Reaction for Rapid and Automated Quantitation of Messenger RNA in Multiple Samples.

Background: Competitive reverse transcription polymerase chain reaction (RT-PCR) has been used increasingly to quantitate messenger RNA (mRNA) levels; however, conventional competitive RT-PCR methods require four or five reactions per sample of RNA, employing serial dilutions of an internal competitor sequence, making analysis of multiple samples of tedious process. A modified method is described by which multiple samples and multiple RNA transcripts can be analyzed easily by an automated process. Methods and Results: Transforming growth factor beta-1 (TGF-beta-1) mRNA was assayed in total RNA extracted from cultured human skin fibroblasts. A standard solution of total RNA was first prepared by pooling RNA from several cell lines and stored in aliquots. A 270-bp competitor RNA molecule (RNA mimic) was prepared by in vitro transcription and was added to each reaction. PCR was performed with a fluorescent dye (Hex; Applied Biosystems, Foster City, CA)-labeled sense primer to amplify a 161-bp-long c DNA product of target TGF-beta-1 mRNA sequence and the RNA mimic. The PCR products were analyzed with an automated laser-scanned gel electrophoresis system and the area under the curve (AUC) was used for quantitation. The concentration TGF-beta-1 mRNA in standard RNA was determined by conventional competitive RT-PCR. Subsequently, equal amounts of RNA mimic were mixed with four serial dilutions of standard RNA and 0.1 µg of sample total RNA for RT-PCR. A standard curve was generated using the known dilutions of a standard target RNA solution and ratio of AUC for target to that for mimic for each dilution. The unknown sample was then quantitated by interpolation of its area under the curve ratio on the standard curve. This method had inter- and intra-assay coefficients of variation of less than 10%. Conclusions: This modification is highly reproducible for quantitation of mRNA and significantly reduces the number of PCR reactions required for each assay. It can be used to assay several RNA molecules in a given sample by designing RNA mimics and PCR primers to generate PCR products of different lengths so that they can be analyzed by the laser scanning of a single lane of electrophoretic gel.

Journal Article↗

Recurrence of haemolytic-uraemic syndrome in renal transplants: a single-centre report.

BACKGROUND: The incidence of recurrence of haemolytic-uraemic syndrome (HUS) in renal allografts appears to vary by centre, with the highest rates reported from the University of Minnesota. It is possible that the high rate of HUS recurrence at this institution reflects a transplant population skewed towards patients with a form of HUS that is more likely to recur in the allograft. METHODS: This study examined whether the initial episode of HUS in the native kidneys was preceded by a diarrhoeal prodrome ('classical HUS') or not ('atypical HUS'), and evaluated transplant outcomes in 24 patients who received 36 transplants at the University of Minnesota between 31 May 1972 and 31 December 1994. RESULTS: Eighteen of the 24 patients had atypical HUS, three had classical HUS, and in three patients the presence or absence of a diarrhoeal prodrome could not be determined. Recurrent HUS, defined as microangiopathic haemolytic anaemia, thrombocytopenia, renal insufficiency, and allograft biopsy findings compatible with HUS, occurred 16 times in 14 grafts in 11 patients. Nine of these patients had atypical HUS, one had classical HUS, and in one the nature of the prodrome could not be determined. Eleven of the 14 initial recurrences took place within 2 months of transplant. Recurrence was not more frequent in patients who received cyclosporin or antilymphocyte preparations. Actuarial analysis using matched controls showed poorer graft survival in patients with a primary diagnosis of HUS (P = 0.007), due to the high frequency of graft loss in HUS patients with recurrence. CONCLUSION: Based upon these data and a review of the literature, it can be concluded that the risk of recurrence of HUS in the allograft is confined almost entirely to patients with atypical forms of HUS.

Adolescent↗

Glomerular volume in congestive cardiac failure.

Glomerular volume has been reported to be increased in patients with congenital cyanotic heart disease and cor pulmonale; however it has not been systematically studied in patients with congestive cardiac failure (CCF). Glomerular volume was therefore measured by point-counting serially sectioned glomerular profiles of 25 randomly selected glomeruli using the Cavalieri principle in autopsy specimens from 8 patients dying from CCF and 6 age-matched controls with no renal or cardiac pathology. Mean glomerular volume was not different between patients dying from CCF and controls, 2.49 (0.21) vs. 2.25 (0.26) x 10(6) microm3, and the distribution of individual glomerular volumes was similar in the two groups. We conclude that severe CCF is not associated with significant glomerular enlargement and that the previously reported glomerular enlargement in cyanotic heart disease is likely to be mediated through hypoxemia.

Acquired Immunodeficiency Syndrome↗

Glomerular changes in normo- and microalbuminuric patients with long-standing insulin-dependent diabetes mellitus.

Normalbuminuric patients who have long-standing IDDM have a wide range of renal structure, from within normal limits to advanced lesions that overlap those of patients who have high levels of MA and border on those seen in patients who have overt DN. Patients who have low-level MA have reduced glomerular structure similar to that of patients who have NA. Low GFR, hypertension, or both can occur in patients who have NA or low-level MA and are associated with more advanced lesions. Patients who have MA and AER greater than 45 mg/24 hr have more advanced lesions than do patients with NA or low-level MA, but similar lesions are present in these patients whether AER is greater than or less than 100 mg/24 hr. Increasing AER in NA and MA patients who have long-standing IDDM is associated with GBM and mesangial expansion. A structural basis for MA cannot currently be deduced from studies of glomerular epithelial cell fine structure, capillary wall charge site analysis, or immunohistochemical studies of renal ECM composition. Hemodynamic adaptations to mesangial expansion and reduced filtration surface and, perhaps, hydraulic conductivity may accelerate glomerular damage, as expressed by increasing AER. Microalbuminuria derives its clinical utility in IDDM, as it identifies a population of patients at statistically increased risk of progression to overt DN by acting as a marker of already well-established DN lesions. Although MA is currently the best of the widely used indicators of DN risk, it is not precise. Therapies that reduce MA may ultimately slow or prevent progression toward ESRD, but this finding requires confirmation by demonstrating that a given treatment strategy can preserve GFR.

Albuminuria↗

Renal structure and function in non-insulin dependent diabetic patients with microalbuminuria.

We have recently described heterogeneity in renal structure in non-insulin-dependent diabetic patients (NIDDM) with microalbuminuria (MA; defined as albumin excretion rate from 20 to 200 micrograms/min). Thus, at variance with IDDM patients, "typical" diabetic glomerulopathy by light microscopy is observed only in a third of NIDDM with MA (Category II, CII). Further, despite persistent MA, 30% of NIDDM have normal or near normal renal structure (Category I, CI). Another one-third shows "atypical" patterns of renal injury with absent or mild diabetic glomerular changes, associated with disproportionately severe tubulointerstitial lesions and/or arteriolar hyalinosis and global glomerular sclerosis (Category III, CIII). The aims of this study were to evaluate whether similar patterns of renal lesions could be confirmed in a larger group of NIDDM with MA and to investigate tubular function in order to understand the mechanisms underlying MA in NIDDM patients. Renal biopsies were performed in 53 NIDDM with MA. Categories I, II and III were found in 41%, 26% and 33% of NIDDM with MA, respectively. All 8 patients with proliferative diabetic retinopathy were in CII. We also studied the urinary daily excretion rate of alpha 1-microglobulin (alpha 1 m), a low molecular weight protein, which is a useful indicator of tubular function. alpha 1 m was markedly increased only in CII patients (CI vs. CII vs. CIII: 6.2 +/- 1.2 vs. 13.7 +/- 2.1 vs. 7.3 +/- 0.9 mg/day, ANOVA, P < 0.01). In conclusion, we confirm that there is heterogeneity in renal structure in NIDDM patients with MA. This heterogeneity is not due to renal diseases other than diabetes. Increased alpha 1 m and proliferative retinopathy are useful indicators of the subgroup of MA NIDDM patients with typical diabetic glomerulopathy. It is suggested that diabetic microangiopathy explains the simultaneous occurrence of typical diabetic glomerulopathy, proliferative retinopathy and tubular dysfunction in a subgroup of NIDDM patients with MA.

Albuminuria↗

Assessment of structure and function in progressive renal disease.

The incidence and prevalence rates of end-stage renal disease (ESRD) in the United States continue to increase. In 1995, the incidence rate was 262 per million population, with a point prevalence rate of 975 per million population. The exact number of individuals with abnormal renal function but not yet at end stage is difficult to assess. Crude estimates suggest that approximately 0.4% of the U.S. population has serum creatinine values greater than 2.0 mg/dl. In some sub-populations, such as African Americans, the estimate is + as high as 1.0%. The rate of progression, likewise, is difficult to assess. In general, renal manifestations of certain systemic diseases such as diabetes mellitus and systemic lupus erythematosus, and those with significant proteinuria (usually greater that 3.0 g/24 hr) seem to have a more rapid progressive course to end stage. If intervention is expected to be successful in halting or slowing down progression, accurate assessment of the early manifestations of renal disease, structure, and function need to be established. Currently accepted methods of assessment of renal disease include measurement of renal function such as serum creatinine and glomerular filtration rate, measurement of proteinuria, assessment of tubular function, glomerular sieving and permselectivity, radiologic imaging techniques, and evaluation of histo-morphometry. Interventions that have been shown to slow progression include control of hypertension, and treatment modalities that reduce proteinuria, such as, the use of angiotensin converting enzyme inhibitors. Further clinical and basic science studies are needed to accurately define the important predictors of progression, and interventions that are effective in slowing or halting progression.

Animals↗

Diabetic nephropathy as a model for the use of renal structural endpoints in clinical trials.

Slowly developing renal diseases (SDRD) such as diabetic nephropathy (DN) and hypertensive nephrosclerosis constitute the large majority of disorders leading to end-stage renal disease (ESRD). These disorders are characterized by years to decades without renal functional abnormalities during which renal structural changes are developing. The earliest renal functional abnormalities [such as microalbuminuria in patients with insulin dependent diabetes mellitus (IDDM)] are often associated with already well established renal lesions that may progress independent of the initiating cause. Since the clinical manifestations of these disorders are dependent upon established structural changes, prevention of the early lesions seems a logical goal and thus a useful endpoint for clinical trials. Functional endpoints are impractical at these early stages as they would take too long to manifest. Diabetic nephropathy in IDDM patients is a useful model for such study design, since there is sufficient knowledge of the natural history of the disorder and of the important structural endpoints to allow for the statistical power calculations crucial for study design. More information regarding natural history and structural-functional relationships is needed in non-insulin dependent diabetes, hypertension, and other SDRD before intervention trials using renal structural endpoints can be developed for these important causes of ESRD.

Animals↗

Patterns of renal injury in NIDDM patients with microalbuminuria.

Microalbuminuria predicts overt nephropathy in non-insulin-dependent diabetic (NIDDM) patients; however, the structural basis for this functional abnormality is unknown. In this study we evaluated renal structure and function in a cohort of 34 unselected microalbuminuric NIDDM patients (26 male/8 female, age: 58 +/- 7 years, known diabetes duration: 11 +/- 6 years, HbA1c: 8.5 +/- 1.6%). Systemic hypertension was present in all but 3. Glomerular filtration rate (GFR) was 101 +/- 27 ml.min-1.1.73 m-2 and albumin excretion rate (AER) 44 (20-199) micrograms/ min. Light microscopic slides were categorized as: C I) normal or near normal renal structure; C II) changes "typical" of diabetic nephropathology in insulin-dependent diabetes (IDDM) (glomerular, tubulo-interstitial and arteriolar changes occurring in parallel); C III) "atypical" patterns of injury, with absent or only mild diabetic glomerular changes associated with disproportionately severe renal structural changes including: important tubulo-interstitial with or without arteriolar hyalinosis with or without global glomerular sclerosis. Ten patients (29.4%) were classified as C I, 10 as C II (29.4%) and 14 as C III (41.2%); none of these patients had any definable non-diabetic renal disease. GFR, AER and blood pressure were similar in the three groups, while HbA1c was higher in C II and C III than in C I patients. Diabetic retinopathy was present in all C II patients (background in 50% and proliferative in 50%). None of the patients in C I and C III had proliferative retinopathy, while background retinopathy was observed in 50% of C I and 57% of C III patients. In summary, microalbuminuric NIDDM patients are structurally heterogeneous with less than one third having "typical" diabetic nephropathology. The presence of both "typical" and "atypical" patterns of renal pathology was associated with worse metabolic control, suggesting that hyperglycaemia may cause different patterns of renal injury in older NIDDM compared to younger IDDM patients.

Aged↗

Active compression-decompression resuscitation: a prospective, randomized study in a two-tiered EMS system with physicians in the field.

Improved cardiopulmonary circulation with active compression-decompression cardiopulmonary resuscitation (ACD-CPR) has been demonstrated in studies using different animal models and a small number of humans in cardiac arrest (CA). However, prehospital studies have shown both positive and no extra benefit of ACD-CPR on return of spontaneous circulation (ROSC), hospital admission and discharge rates. The aim of our prospective study was to compare standard manual CPR (S-CPR) with ACD-CPR as the initial technique of resuscitating patients with out-of-hospital CA, with respect to survival rates and neurological outcome. Patients with out-of-hospital CA treated by emergency medical services (EMS) personnel were randomly assigned to one of two groups (ACD-CPR versus S-CPR). Time intervals to key measures were documented by means of on-line tape-recording. Neurological outcome was assessed using standard scoring systems (cerebral and overall performance categories (CPC and OPC)). A total of 220 patients (S-CPR, n = 114: ACD-CPR, n = 106) were included in the study in a random order. The treatment groups were similar with respect to age, sex, time interval from collapse to CPR, defibrillation and first adrenaline medication. There was no difference between the ACD group and the standard CPR group in terms of ROSC (50.9% vs. 59.6%), hospital admission (33% vs. 33.3%), hospital discharge (16% vs. 14%), or CPC and OPC (1.82 vs. 2.13 and 2.06 vs. 2.25, respectively). Concerning complications of CPR, there was no difference between the groups. In our two-tiered EMS system with physician-staffed ambulances, ACD-CPR neither improved nor impaired survival rates and neurological prognosis in patients with out-of-hospital cardiac arrest. The new CPR technique did not increase the complications associated with the resuscitation effort.

Cardiopulmonary Resuscitation↗