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Electrocardiographic characteristics and catheter ablation of parahissian accessory pathways.

BACKGROUND: Accessory pathways may be located in close proximity to the His bundle, resulting in a high risk of heart block during attempted surgical or electrical interruption of these pathways. This study reports the prevalence, ECG characteristics, and results of catheter ablation of parahissian accessory pathways. They were defined on the basis of both the presence of a high amplitude (> 0.1 mV) of His bundle potential at the ablation site and an exclusion of anteroseptal or midseptal location of the accessory pathway. METHODS AND RESULTS: Eight patients with a parahissian accessory pathway were identified among 582 consecutive patients who underwent radiofrequency ablation of an accessory pathway. They were six males and two females with a mean age of 21 +/- 9 years. During maximal preexcitation, the ECG showed a positive delta wave in leads I, II, and a VF in all patients: six had a negative delta wave in leads V1 and V2 instead of the positivity usually observed in anteroseptal accessory pathways. This pattern had a sensitivity of 75%, a specificity of 96%, a positive predictive value of 86%, and a negative predictive value of 93% for a parahissian location in comparison with a group of 28 patients with anteroseptal accessory pathways. At the successful ablation site, the mean amplitude of the His bundle potential was 0.2 +/- 0.1 (0.12 to 0.4 mV). All accessory pathways were successfully ablated without causing heart block using 5 to 20 W of radiofrequency energy. CONCLUSIONS: Parahissian accessory pathways have a preexcitation pattern that is distinctive from that of anteroseptal accessory pathways. Catheter ablation of these pathways is feasible using low energy with preservation of normal atrioventricular conduction.

Adolescent↗

Glucose-potentiated chemotaxis in human vascular smooth muscle is dependent on cross-talk between the PI3K and MAPK signaling pathways.

Atheroma formation involves the movement of vascular smooth muscle cells (VSMC) into the subendothelial space. The aim of this study was to determine the involvement of PI3K and MAPK pathways and the importance of cross-talk between these pathways, in glucose-potentiated VSMC chemotaxis to serum factors. VSMC chemotaxis occurred in a serum gradient in 25 mmol/L glucose (but not in 5 mmol/L glucose) in association with increased phosphorylation (activation) of Akt and ERK1/2 in PI3K and MAPK pathways, respectively. Inhibitors of these pathways blocked chemotaxis, as did an mTOR inhibitor. VSMC expressed all class IA PI3K isoforms, but microinjection experiments demonstrated that only the p110beta isoform was involved in chemotaxis. ERK1/2 phosphorylation was reduced not only by MAPK pathway inhibitors but also by PI3K and mTOR inhibitors; when PI3K was inhibited, ERK phosphorylation could be induced by microinjected activated Akt, indicating important cross-talk between the PI3K and ERK1/2 pathways. Glucose-potentiated phosphorylation of molecules in the p38 and JNK MAPK pathways inhibited these pathways but did not affect chemotaxis. The statin, mevinolin, blocked chemotaxis through its effects on the MAPK pathway. Mevinolin-inhibited chemotaxis was restored by farnesylpyrophosphate but not by geranylgeranylpyrophosphate; in the absence of mevinolin, inhibition of farnesyltransferase reduced ERK phosphorylation and blocked chemotaxis, indicating a role for the Ras family of GTPases (MAPK pathway) under these conditions. In conclusion, glucose sensitizes VSMC to serum, inducing chemotaxis via pathways involving p110beta-PI3K, Akt, mTOR, and ERK1/2 MAPK. Cross-talk between the PI3K and MAPK pathways is necessary for VSMC chemotaxis under these conditions.

Alkyl and Aryl Transferases↗

Automation of gene assignments to metabolic pathways using high-throughput expression data.

BACKGROUND: Accurate assignment of genes to pathways is essential in order to understand the functional role of genes and to map the existing pathways in a given genome. Existing algorithms predict pathways by extrapolating experimental data in one organism to other organisms for which this data is not available. However, current systems classify all genes that belong to a specific EC family to all the pathways that contain the corresponding enzymatic reaction, and thus introduce ambiguity. RESULTS: Here we describe an algorithm for assignment of genes to cellular pathways that addresses this problem by selectively assigning specific genes to pathways. Our algorithm uses the set of experimentally elucidated metabolic pathways from MetaCyc, together with statistical models of enzyme families and expression data to assign genes to enzyme families and pathways by optimizing correlated co-expression, while minimizing conflicts due to shared assignments among pathways. Our algorithm also identifies alternative ("backup") genes and addresses the multi-domain nature of proteins. We apply our model to assign genes to pathways in the Yeast genome and compare the results for genes that were assigned experimentally. Our assignments are consistent with the experimentally verified assignments and reflect characteristic properties of cellular pathways. CONCLUSION: We present an algorithm for automatic assignment of genes to metabolic pathways. The algorithm utilizes expression data and reduces the ambiguity that characterizes assignments that are based only on EC numbers.

Algorithms↗

Computational prediction of human metabolic pathways from the complete human genome.

BACKGROUND: We present a computational pathway analysis of the human genome that assigns enzymes encoded therein to predicted metabolic pathways. Pathway assignments place genes in their larger biological context, and are a necessary first step toward quantitative modeling of metabolism. RESULTS: Our analysis assigns 2,709 human enzymes to 896 bioreactions; 622 of the enzymes are assigned roles in 135 predicted metabolic pathways. The predicted pathways closely match the known nutritional requirements of humans. This analysis identifies probable omissions in the human genome annotation in the form of 203 pathway holes (missing enzymes within the predicted pathways). We have identified putative genes to fill 25 of these holes. The predicted human metabolic map is described by a Pathway/Genome Database called HumanCyc, which is available at http://HumanCyc.org/. We describe the generation of HumanCyc, and present an analysis of the human metabolic map. For example, we compare the predicted human metabolic pathway complement to the pathways of Escherichia coli and Arabidopsis thaliana and identify 35 pathways that are shared among all three organisms. CONCLUSIONS: Our analysis elucidates a significant portion of the human metabolic map, and also indicates probable unidentified genes in the genome. HumanCyc provides a genome-based view of human nutrition that associates the essential dietary requirements of humans with a set of metabolic pathways whose existence is supported by the human genome. The database places many human genes in a pathway context, thereby facilitating analysis of gene expression, proteomics, and metabolomics datasets through a publicly available online tool called the Omics Viewer.

Arabidopsis↗

The methylerythritol phosphate pathway and its significance as a novel drug target.

Isopentenyl diphosphate (IPP) and dimethylallyl diphosphate (DMAPP) are the precursors for all isoprenoid compounds. Two pathways are found in Nature for their biosynthesis. The mevalonate (MVA) pathway is found in eukaryotes, algae, archae and some gram-positive bacteria. Gram-negative bacteria, plants and some gram-positive bacteria utilize the methyl erythritol phosphate (MEP) pathway. The distribution and the orthogonal nature of the pathways make the MEP pathway an attractive new target for antibiotics and herbicides. The MEP pathway is essential for bacterial viability. Inhibitors to the MEP pathway represent a "dual-use technology" because potential targets include potential biological warfare agents in addition to common human pathogens. The CDC has three categories designated for Biological Diseases/Agents. Three of the six entities designated as the highest priority (Category A) are organisms that utilize, or appear to utilize, the MEP pathway. Among the 12 second highest priority agents (Category B) listed, 8 are organisms that appear to utilize the MEP pathway. Common human pathogens that can be targeted include the organisms responsible for peptic ulcers, tuberculosis, malaria, food safety threats, and sexually transmitted diseases. There is so far only one inhibitor reported that specifically blocks the MEP pathway and is being investigated clinically. This compound, fosmidomycin, has been shown to be somewhat effective in treating Plasmodium falciparum, the parasite responsible for malaria. We foresee that new MEP pathway inhibitors will open up an entirely new class of antibiotics. An MEP pathway intermediate has also been shown to be the most potent gammadelta T cell activator.

Animals↗

Vital elements of the Wnt-Frizzled signaling pathway in the nervous system.

Wnt proteins are cysteine-rich glycosylated proteins named after the Drosophilia Wingless (Wg) and the mouse Int-1 genes that play a role in embryonic cell patterning, proliferation, differentiation, orientation, adhesion, survival, and programmed cell death (PCD). Wnt proteins involve at least two intracellular signaling pathways. One pathway controls target gene transcription through beta-catenin, generally referred to as the canonical pathway and a second pathway pertains to intracellular calcium (Ca(2+)) release which is termed the non-canonical or Wnt/ Ca(2+) pathway. The majority of Wnt proteins activate gene transcription through the canonical signaling pathway regulated by pathways that include the Frizzled transmembrane receptor and the co-receptor LRP-5/6, Dishevelled, glycogen synthase kinase-3beta (GSK-3beta), adenomatous polyposis coli (APC), and beta-catenin. In contrast, the non-canonical Wnt signaling pathway has two intracellular signaling cascades that consist of the Wnt/ Ca(2+) pathway with protein kinase C (PKC) and the Wnt/PCP pathway involving Rho/Rac small GTPase and Jun N-terminal kinase (JNK). Through a series of signaling pathways, Wnt proteins modulate cell development, proliferation, and cell fate. In regards to cell survival and fate through PCD, Wnt may be critical for the prevention of tissue pathology that involves cytokine and growth factor control during disorders such as neuropsychiatric disease, retinal disease, and Alzheimer's disease. Elucidation of the vital elements that shape and control the Wnt-Frizzled signaling pathway may provide significant prospects for the treatment of disorders of the nervous system.

Animals↗

[Phase 3 and phase 4 block in the accessory pathway].

Pacemaker activity at a site proximal to the area of a conduction disturbance has been postulated as depressing conduction in late diastole (phase 4 block). To elucidate the correlation between the site of phase 4 depolarization and that of a conduction disturbance, we examined seven patients with intermittent Wolff-Parkinson-White syndrome who had tachycardia (phase 3) and bradycardia (phase 4) dependent on block in the accessory pathway. In each patient, antegrade conduction over the accessory pathway was absent at the sinus rate. During premature atrial stimulation a "window" of accessory pathway conduction was identified in each patient. The outer limit of the window ranged from 420 to 670 ms; the inner limit, from 330 to 620 ms. The duration of the window ranged from 20 to 160 ms. Four patients with orthodromic atrioventricular reentrant tachycardia exhibited preserved retrograde accessory pathway conduction. In one patient with unsustained orthodromic atrioventricular reentrant tachycardia, retrograde accessory pathway conduction also exhibited phase 3 and phase 4 blocks. The remaining two patients had no retrograde accessory pathway conduction. In two patients, retrograde concealed conduction in the accessory pathway induced by ventricular stimulation eliminated a phase 4 block in antegrade accessory pathway conduction. These results suggest that 1) an antegrade phase 4 block may have phase 4 depolarization in the accessory pathway and block at the ventricular insertion of the accessory pathway; 2) a retrograde phase 4 block may have a conduction disturbance at the atrial insertion of the accessory pathway; and 3) a complete retrograde block may occur at the atrial insertion of the accessory pathway.

Adolescent↗

The role of the capsular polysaccharide in the activation of the alternative pathway by the pneumococcus.

Previous studies have shown that when pneumococci are incubated in normal, nonimmune serum, they activate the alternative pathway and opsonically active C3b is fixed to the surface of the organism. Other studies have demonstrated that C3-dependent opsonization via the alternative pathway plays a significant role in the nonimmune host's defense against the pneumococcus. The present studies concern the role of the capsular polysaccharide in initiating the activation of the alternative pathway by the pneumococcus. Some pneumococcal capsular polysaccharide types, but not all, are able to activate the alternative pathway. Soluble purified capsular polysaccharide types 1, 4 and 25 activate the alternative pathway, whereas types 2, 3, 14, and 19 do not. Since the capsular polysaccharides exist in their native form attached to the pneumococcal surface, selected capsular polysaccharides were also tested for their ability to activate the alternative pathway when attached to a particulate carrier, sheep erythrocytes. Capsular polysaccharide types 2 and 3 failed to activate the alternative pathway when attached to sheep erythrocytes, paralleling the results obtained when these capsular polysaccharides were in solution. In contrast, the type 25 capsular polysaccharide not only activated the alternative pathway when attached to sheep erythrocytes, as it had when in solution, but it also initiated alternative pathway-mediated lysis of the erythrocytes. The capsular polysaccharide is not required for the activation of the alternative pathway by the pneumococcus. Although all types of encapsulated pneumococci are able to activate the alternative pathway, not all the purified capsular polysaccharide types are able to do so. In addition, a nonencapsulated pneumococcus, derived originally from a type 2 organism, activates the alternative pathway as well as a fully encapsulated type 2 pneumococcus.

Cell Wall↗

Early events in initiation of alternative complement pathway activation by the capsule of Cryptococcus neoformans.

The capsule of Cryptococcus neoformans is a powerful activator of the alternative complement pathway. This study examined the manner in which the cryptococcal capsule influences initiation of and early events in complement activation by C. neoformans. These studies examined the effects of the classical and alternative pathways on the kinetics and early sites for deposition of C3 fragments on encapsulated cryptococci, nonencapsulated cryptococci, and zymosan. The results showed that nonencapsulated cryptococci and zymosan are qualitatively and quantitatively similar in the manner in which they initiate complement activation. Both utilize the classical and alternative pathways. Initiation via the classical pathway occurs suddenly and simultaneously at sites distributed over the entire cell surface. Initiation of the alternative pathway by zymosan and nonencapsulated cryptococci is characterized by a lag of 6 to 8 min before appreciable amounts of C3 accumulate on the cells. Alternative pathway initiation by zymosan and nonencapsulated cryptococci occurs at a limited number of focal initiation sites that expand with alternative pathway amplification to cover the cell surface. Presence of the cryptococcal capsule blocks classical pathway initiation, which would normally occur at the cryptococcal cell wall, and produces an initiation that is dependent solely on the alternative pathway. Initiation of the alternative pathway by the cryptococcal capsule is characterized by a lag in C3 accumulation and the appearance of a limited number of focal initiation sites which resemble those observed when the alternative pathway is activated by zymosan and nonencapsulated cryptococci.

Complement Activation↗

The inhibitory effect of factor J on the alternative complement pathway.

Factor J (FJ) is a cationic glycoprotein with inhibitory activity in C1, the first component of the classical complement pathway. This study demonstrates that FJ is able to regulate the activity of the alternative complement pathway. FJ inhibits the generation of fluid-phase and cell-bound alternative pathway C3 convertase, C3b,Bb (C3-cleaving enzyme). Thus, FJ interferes with the generation of alternative pathway C3 convertase when sheep erythrocytes bearing antibody and activated C3 and C4 (EAC4b,3b) are incubated with the individual complement components, factors B, D, and P. FJ accelerates the decay of C3 convertase with a time course similar to that of factor H, and when both regulators are present together, the decay of enzyme activity is faster than when they are added separately. Furthermore, FJ is able to inhibit the cleavage of C3 by factor B in a fluid-phase assay. FJ prevents the initiation of alternative pathway activation in "more stabilized systems" with well known activators of alternative pathway C3 convertase such as C3 nephritic factor (an autoantibody against alternative pathway C3 convertase), cobra venom factor, and rabbit erythrocytes. In these systems, FJ has no effect on C3 convertase stabilized by rabbit erythrocytes or cobra venom factor. In contrast, FJ promotes the dissociation of C3 convertase stabilized by C3 nephritic factor, but with much lower efficiency than in preventing initiation. Direct interaction of FJ with individual components of C3 convertase was shown by a solid-phase binding assay using plates coated with C3, C3b, B, Bb, or FJ. FJ inhibitory activity in the alternative pathway can be modulated by polyanions like heparin. FJ-mediated inhibition in the alternative complement pathway can be modified by surface interactions, as occurs during alternative pathway C3 convertase activation. Thus, when FJ is adsorbed by and eluted from hydroxylapatite and reverse-phase columns, its inhibitory effect on more stabilized systems is lost. This loss of inhibitory activity is fully reversed when FJ is rechromatographed on heparin-Sepharose or Sepharose columns. Taking into account these data, FJ may be included in the group of highly charged molecules that inhibit the activation of classical and alternative complement pathways (i.e. eosinophil major basic protein, protamine, and heparin).

Animals↗

The impact of clinical pathways on the practice of head and neck oncologic surgery: the University of Texas M. D. Anderson Cancer Center Experience.

OBJECTIVE: To assess the impact of clinical pathways on the practice of head and neck oncologic surgery in an academic center. DESIGN: Cross-sectional study. SETTING: Cancer treatment center. PATIENTS: The study population consisted of 3 groups of patients who underwent unilateral neck dissection and were treated in the Department of Head and Neck Surgery of the University of Texas M. D. Anderson Cancer Center, Houston. Additional procedures which may have been performed were direct laryngoscopy, rigid esophagoscopy, and/or dental extractions. Ninety-six patients treated during 1993-1994 prior to the implementation of the clinical pathway (historical control group) were compared with 94 patients treated during 1996-1998, 64 who were not (contemporaneous nonpathway group) and 30 who were managed on the clinical pathway (pathway group). Patients from 1995 were excluded since the pathway was in the planning stages then. MAIN OUTCOME MEASURES: Median length of stay; median total costs of care. RESULTS: The median length of hospital stay of the historical control, contemporaneous nonpathway, and pathway groups decreased from 4.0 to 2.0 days (P<.001). The total median costs of care were less in the pathway group as compared with the historical control group ($6,227 and $8,459, respectively, P<.001) and also less in the contemporaneous nonpathway group compared with the historical control group (S6885 and $8,459, respectively, P<.001). Mean and median length of hospital stay and costs were lower in the pathway group as compared with the nonpathway group but not significantly (P = .11 and P = .07, respectively) The contemporaneous nonpathway and pathway groups did not differ in complications or readmissions. CONCLUSIONS: Development and implementation of this clinical pathway played a statistically significant role in decreasing length of hospital stay and total costs of care associated with neck dissection between nonpathway and pathway patients. Thus, a more cost-effective practice environment has resulted for all of our patients.

Academic Medical Centers↗

Antibody-mediated activation of the classical pathway of complement may compensate for mannose-binding lectin deficiency.

Deficiency of mannose-binding lectin (MBL), a recognition molecule of the lectin pathway of complement, is associated with increased susceptibility to infections. The high frequency of MBL deficiency suggests that defective MBL-mediated innate immunity can be compensated by alternative defense strategies. To examine this hypothesis, complement activation by MBL-binding ligands was studied. The results show that the prototypic MBL ligand mannan can induce complement activation via both the lectin pathway and the classical pathway. Furthermore, antibody binding to mannan restored complement activation in MBL-deficient serum in a C1q-dependent manner. Cooperation between the classical pathway and the lectin pathway was also observed for complement activation by protein 60 from Listeria monocytogenes. MBL pathway analysis at the levels of C4 and C5b-9 in the presence of classical pathway inhibition revealed a large variation of MBL pathway activity, depending on mbl2 gene polymorphisms. MBL pathway dysfunction in variant allele carriers is associated with reduced MBL ligand binding and a relative increase of low-molecular-mass MBL. These findings indicate that antibody-mediated classical pathway activation can compensate for impaired target opsonization via the MBL pathway in MBL-deficient individuals, and imply that MBL deficiency may become clinically relevant in absence of a concomitant adaptive immune response.

Antibodies↗

Development and regenerative capacity of descending supraspinal pathways in tetrapods: a comparative approach.

Throughout tetrapods a basic pattern in the organization of descending supraspinal pathways is present. The most notable difference between nonmammalian tetrapods and mammals is the apparent absence of somatomotor cortical areas giving rise to long descending projections to the spinal cord. The phylogenetic constancy of descending supraspinal pathways, at least of those arising in the brain stem, probably implies a comparable pattern of development, presumably a developmental sequence in the formation of these central motor pathways. For studies on the development of motor systems, anurans such as the clawed toad, Xenopus laevis, chicken embryos, and opossums are very attractive animals. Moreover, in these species as well as in rodents in vitro approaches can be used. In the present survey, current knowledge on the neurogenesis, axonal outgrowth, synaptogenesis, and developmental plasticity of the central motor pathways in tetrapods including the sparse data available for man, is discussed. These data are placed in the perspective of the development of the spinal cord and, where possible, correlated with functional data. Emphasis is on the clawed toad, X. laevis, chicken embryos, and opossum and rodent data. The outgrowth of axons of descending supraspinal pathways can be regarded as the result of a series of distinct processes, which may be expressed in a coordinated program: (1) the outgrowth of axons and selection of pathways to their appropriate destination; (2) dendritic outgrowth and formation of specific dendritic morphology; (3) selection of specific targets and collateralization by axons; (4) elimination of incorrect and redundant synapses, axonal and dendritic branches, and of mismatched neurons; and (5) functional refinement of synaptic connections. Tracer and transmitter immunohistochemistry in Xenopus laevis showed that from the moment cell division stops, an axon is formed followed by dendrites which emerge from the cell body. At the beginning of the cell differentiation phase the production of the cell-specific neuroactive substances takes place. Initial outgrowth is in a specific direction for each class of neuron. It is likely that all descending supraspinal pathways arise in a similar way. In the spinal projections of each of the descending supraspinal pathways three stages can be distinguished: (1) an initial stage of outgrowth to the spinal cord, (2) a short "waiting" period after which collaterals enter the spinal gray matter, and (3) myelination of axons. An "overshoot" of spinal projections is particularly evident for the mammalian corticospinal tract. The pattern of early descending axonal tracts appears to be similar in all vertebrate groups. Early axons lay down an axonal scaffold containing guidance cues that are available to later generated growth cones. Throughout vertebrates including man, the fasciculus longitudinalis medialis (flm) is the first descending pathway to be formed. Interstitiospinal fibers "pioneer" this tract, and are joined by reticulospinal fibers. Vestibulospinal fibers (the medial vestibulospinal tract) follow much later. The lateral vestibulospinal tract takes a separate course through the brain stem. Late-arriving fiber tracts such as the rubrospinal and corticospinal tracts probably have their own mechanism of selecting the appropriate pathway. The formation of the descending supraspinal pathways occurs according to a developmental sequence. In all tetrapods studied, reticulospinal and interstitiospinal fibers reach the spinal cord first, followed by vestibulospinal fibers and, much later, by rubrospinal and, if present, corticospinal projections. A special case is presented by anurans which in fact have two motor systems, a primary, transient motor system and a secondary, definitive motor system. Reticulospinal, interstitiospinal and vestibulospinal fibers innervate the spinal cord very early in development, well before the development of the hindlimbs. Rubrospinal fibers in

Animals↗

Electrophysiologic study demonstrating triple antegrade AV nodal pathways in patients with spontaneous and/or induced supraventricular tachycardia.

Ten patients are described with two discrete discontinuities in AV nodal conduction curves suggesting triple antegrade AV nodal pathways. This represents approximately 6% of patients seen in this laboratory with dual AV nodal pathways. Patients ranged in age from 18 to 63 (mean +/- SD, 48 +/- 15 years). Six of the 10 patients had organic heart disease and four did not. The effect of cycle length on triple pathways could be analyzed in 8 of 10 patients who had atrial extrastimulus testing at two or more cycle lengths. Three of these eight patients had triple pathways at all tested cycle lengths. Four patients had triple pathways only at shorter cycle lengths. One patient had triple pathways only at longer cycle lengths. Intact retrograde conduction was demonstrated in seven of ten patients, all of whom had atrial echoes (two patients) or inducible supraventricular tachycardia (SVT) (five patients). Echoes or SVT were induced on the slow pathway is all seven patients, but also on the intermediate pathway in three. However, sustained SVT usually reflected antegrade slow and retrograde fast pathway conduction. In conclusion, triple AV nodal pathways may be demonstrated in occasional patients during atrial extrastimulus testing. Thereby, functional longitudinal dissociation of the AV node is not limited to two pathways.

Adolescent↗

Clinical pathways in home nutrition support.

In home-care settings, physicians with various medical specialties may order home enteral and/or parenteral nutrition support. Clinical pathways may be used to provide a clear, concise, standardized method for ordering and monitoring home nutrition support. The clinical pathways should be appropriate for 80% of the patients placed on the pathways, allowing for a 20% variance, or deviation, from the pathway. In one home-care facility, disease-specific clinical pathways have been used for longer than 1 year for patients with a variety of diseases requiring home nutrition support. To determine the usefulness of the home nutrition support clinical pathways, data obtained from 20 patients were analyzed. Patients were followed up while being treated using home nutrition support clinical pathways designed for oncology (9 patients), human immunodeficiency virus/acquired immunodeficiency syndrome (2 patients), short bowel syndrome (6 patients), and hyperemesis (3 patients) for 191 weeks. Overall, an average variance (deviation from the pathway) of 22% (the number of variances divided by the total weeks of therapy) was observed. The use of the pathways to provide enteral or parenteral nutrition facilitated more cost-effective care by following pathway guidelines for obtaining laboratory values and patient visits. Communication between the home-care staff and the physician was also improved. Clinical pathways can enable standardization of care for patients receiving nutrition support at home.

Critical Pathways↗

Impact of a critical pathway on postoperative length of stay and outcomes after infrainguinal bypass.

PURPOSE: To determine the effect of a critical pathway on postoperative length of stay and outcomes after infrainguinal bypass. METHODS: A critical pathway for care of patients after infrainguinal bypass was introduced in December 1995 to coordinate postoperative care at our institution. We compared care of 67 consecutively treated patients before institution of the pathway with care of 69 consecutively treated patients with the critical pathway in place. Data collection was done by means of chart review. Univariate analyses were used to identify differences between prepathway and postpathway patients and to identify factors influencing postoperative length of stay. Multivariate analysis was used to identify factors that influenced length of stay and to examine the effect of use of the pathway after adjusting for other factors. RESULTS: Patients on the pathway were similar to prepathway controls with respect to comorbid illnesses, vascular risk factors, indications for surgical treatment, type of conduit, and type of operation. Factors associated with longer postoperative stays included distal anastomoses to tibial rather than popliteal vessels (p = 0.02), preexisting cardiac disease (p = 0.005), postoperative complications (p = 0.0003), lower preoperative hematocrit (p = 0.01), and elevated preoperative creatinine level (p = 0.006). Overall, pathway patients had somewhat shorter postoperative lengths of stay (median value 7 days; range 2 to 29 days) than prepathway patients (median value 6 days; range 2 to 35; p = 0.01), and the two groups had similar frequencies of postoperative complications, readmission, and 6-month mortality. However, patients on the pathway were more likely to be discharged to an intermediate-care facility rather than directly home. After 12 patients with extraordinarily prolonged postoperative stays were excluded, multivariate analysis indicated that pathway patients had significantly shorter postoperative stays (p = 0.001). However, the difference was not significant if patients with extraordinarily long postoperative stays were included in the analysis (p = 0.28). CONCLUSION: Use of a critical pathway was associated with a modest decrease in postoperative length of stay for most patients. This was accomplished without an adverse effect on readmission, complication, or mortality rates. However, the decrease in stay may have been achieved primarily by discharging more patients to intermediate-care facilities. The pathway did not appear to have any effect when the subset of patients with extraordinarily long stays because of complex medical problems was included.

Aged↗

[Design, implementation, and results of the clinical pathway for herniated lumbar disk].

INTRODUCTION: Clinical or critical pathways are a useful tool in the continuous quality improvement. They develop the main characteristics of the quality programs: implementation of the evidence based medicine, increase staff and patient satisfaction and adequacy in hospital costs. This is the application of evidence-based medicine to a process management and it promotes integration of clinical guides, protocols and algorithms. OBJECTIVE: We present our experience in the design, and first nine month's implementation and development of a clinical pathway for lumbar hemilaminectomy. PATIENTS AND METHODS: This clinical pathway consists on four documents: main guide and check sheet, preprinted treatment orders and variation sheet, iconographic information for the patients and patient satisfaction questionnaire. After desing, development and a pilot study, the hemilaminectomy critical pathway was permanently adopted by our Service. A total of 106 patients underwent programmed lumbar disc hemilaminectomy in our Service between April and December-1999. Patients' average age was 44.7 years (SD = 11.2), 55.3% were men and 43.7% women. Twelve were hospitalized in a ward other than Neurosurgery unit and therefore were excluded from the study. This evaluation is based on the initial results obtained from both the pathway documents and the general data collected as usual during hospital care. The impact of the critical pathway on hospital stay has been assessed by comparing the average stay of critical pathway patients to the average of the 70 hemilaminectomies performed at our Service in the period April-December 1998. RESULTS: Clinical pathway coverage has been 68% (standard > 80%). The patients' average stay was 4 days (SD = 1.1), one day more than planned. The pathway establishes a 4 day hospital stay (3 bed-days), a time that was fulfilled by 49% of the patients. The average stay of the 1998 patients was 5.6 days (SD = 2.7), 1.6 days more than the clinical pathway patients (p < 0.0001). Additionally, undesirable variability in the length of hospital stays was also reduced. Analysis of variations identified those corresponding to patient's condition, increases in medication beyond that originally specified due to patient needs, and unjustified prolonged stays. There were no systematic variations. There was a 2.2% incidence of adverse effects. Although satisfaction questionnaire was only returned by 51% of the patients (instead of > 70%), satisfaction index were 93% (vs 90%). CONCLUSIONS: Critical pathways are still under development and changing continuously. Nevertheless their impact on improving patient care and satisfaction, and resource consumption is already evident, and it constitutes a major aim to work in its complete development.

Adolescent↗

[Clinical pathways -- first results of a systematic IT-supported application at a surgical department of a university hospital].

BACKGROUND AND OBJECTIVE: In analogy to industrial process management, clinical pathways have been introduced for operational process organisation in orthopedic and interventional procedures as well as for conservative treatments. Within this study, introduction and continuous, systematic application of clinical pathways at a surgical department of a university hospital was investigated. METHODS: Analysis was performed by IT-based (SAP/i. s. h.med) evaluation of the registered data regarding pathway violations. Additionally, patients' records were matched with the computerized data for quality assurance of pathway documentation. RESULTS: 501 patients were entered in 16 clinical pathways (31 +/- 39 patients per pathway). The mean period from the introduction of a distinct pathway to the data acquisition of the present study ranged from 2 to 14 months (mean 7+/-7.5 months). Pathway violations correlated with the complexity, but not with the period since the pathway was introduced. Organisational reasons next to medical reasons (i. e. delayed gastric function or wound healing) were the most frequent causes for pathway violations. CONCLUSION: Clinical pathways may not only be realised for operative procedures or conservative treatments, but represent a clinical and administrative management instrument at a surgical department of a university hospital for daily work routine. They are suitable as an instrument for clinical quality and risk management, as an economic control instrument in reorganisation phases as well as in the routine of surgical clinics.

Critical Pathways↗