Biomedical subjects

J Pavlin

Publications and source records attributed to J Pavlin.

8 recordsLinked to original sources

PubMed2005

Implementation of laboratory order data in BioSense Early Event Detection and Situation Awareness System.

INTRODUCTION: Laboratory test orders constitute an early outbreak data source. CDC receives laboratory order data in HL7 format from the Laboratory Corporation of America (LabCorp) and plans to use the data in the BioSense Early Event Detection and Situation Awareness System. METHODS: These LabCorp data contain information on tests ordered and include the type of test ordered and the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM)-coded reasons for the order. A consensus panel was formed to group test orders on the basis of expert opinion into eight standard syndrome categories to provide an additional data source for early outbreak detection. A laboratory order taxonomy was developed and used in the mapping consolidation phase. The five main classes of this taxonomy are miscellaneous functional tests, fluid screening tests, system-specific tests, tests for specific infections (by primary manifestation), and tests for specific noninfectious diseases. RESULTS: Summary of numbers of laboratory order codes in each syndrome category are fever (53), respiratory (53), gastrointestinal (27), neurological (35), rash (37), lymphadenitis (20), localized cutaneous lesion (11), and specific infection (63). CONCLUSION: With the daily use of laboratory order data in BioSense, the actual distribution of laboratory order codes in syndrome groups can be evaluated, allowing modification of the mapping.

Clinical Laboratory Information Systems↗

PubMed2005

An evaluation model for syndromic surveillance: assessing the performance of a temporal algorithm.

INTRODUCTION: Syndromic surveillance offers the potential to rapidly detect outbreaks resulting from terrorism. Despite considerable experience with implementing syndromic surveillance, limited evidence exists to describe the performance of syndromic surveillance systems in detecting outbreaks. OBJECTIVES: To describe a model for simulating cases that might result from exposure to inhalational anthrax and then use the model to evaluate the ability of syndromic surveillance to detect an outbreak of inhalational anthrax after an aerosol release. METHODS: Disease progression and health-care use were simulated for persons infected with anthrax. Simulated cases were then superimposed on authentic surveillance data to create test data sets. A temporal outbreak detection algorithm was applied to each test data set, and sensitivity and timeliness of outbreak detection were calculated by using syndromic surveillance. RESULTS: The earliest detection using a temporal algorithm was 2 days after a release. Earlier detection tended to occur when more persons were infected, and performance worsened as the proportion of persons seeking care in the prodromal disease state declined. A shorter median incubation state led to earlier detection, as soon as 1 day after release when the incubation state was < or =5 days. CONCLUSION: Syndromic surveillance of a respiratory syndrome using a temporal detection algorithm tended to detect an anthrax attack within 3-4 days after exposure if >10,000 persons were infected. The performance of surveillance (i.e., timeliness and sensitivity) worsened as the number of persons infected decreased.

Algorithms↗

PubMed2004

Evaluation of syndromic surveillance systems--design of an epidemic simulation model.

INTRODUCTION: The paucity of outbreak data from biologic terrorism and emerging infectious diseases limits the evaluation of syndromic surveillance systems. Evaluation using naturally occurring outbreaks of proxy disease (e.g., influenza) is one alternative but does not allow for rigorous evaluation. Another approach is to inject simulated outbreaks into real background data, but existing simulation models generally do not account for such factors as spatial mobility and do not explicitly incorporate knowledge of the disease agent. OBJECTIVE: The objective of this analysis was to design a simulated anthrax epidemic injection model that accounts for the complexity of the background data and enables sensitivity analyses based on uncertain disease-agent characteristics. MODEL REQUIREMENTS AND ASSUMPTIONS: Model requirements are described and used to limit the scope of model development. Major assumptions used to limit model complexity are also described. Available literature on inhalational anthrax is reviewed to ensure that the level of model detail reflects available disease knowledge. MODEL DESIGN: The model is divided into four components: 1) agent dispersion, 2) infection, 3) disease and behavior, and 4) data source. The agent-dispersion component uses a Gaussian plume model to compute spore counts on a fine grid. The infection component uses a cohort approach to identify infected persons by residential zip code, accounting for demographic covariates and spatial mobility. The disease and behavior component uses a discrete-event approach to simulate progression through disease stages and health-services utilization. The data-source component generates records to insert into background data sources. CONCLUSIONS: An epidemic simulation model was designed to enable evaluation of syndromic surveillance systems. The model addresses limitations of existing simulation approaches by accounting for such factors as spatial mobility and by explicitly modeling disease knowledge. Subsequent work entails software implementation and model validation.

Anthrax↗

PubMed2004

Bio-ALIRT biosurveillance detection algorithm evaluation.

INTRODUCTION: Early detection of disease outbreaks by a medical biosurveillance system relies on two major components: 1) the contribution of early and reliable data sources and 2) the sensitivity, specificity, and timeliness of biosurveillance detection algorithms. This paper describes an effort to assess leading detection algorithms by arranging a common challenge problem and providing a common data set. OBJECTIVES: The objectives of this study were to determine whether automated detection algorithms can reliably and quickly identify the onset of natural disease outbreaks that are surrogates for possible terrorist pathogen releases, and do so at acceptable false-alert rates (e.g., once every 2-6 weeks). METHODS: Historic de-identified data were obtained from five metropolitan areas over 23 months; these data included International Classification of Diseases, Ninth Revision (ICD-9) codes related to respiratory and gastrointestinal illness syndromes. An outbreak detection group identified and labeled two natural disease outbreaks in these data and provided them to analysts for training of detection algorithms. All outbreaks in the remaining test data were identified but not revealed to the detection groups until after their analyses. The algorithms established a probability of outbreak for each day's counts. The probability of outbreak was assessed as an "actual" alert for different false-alert rates. RESULTS: The best algorithms were able to detect all of the outbreaks at false-alert rates of one every 2-6 weeks. They were often able to detect for the same day human investigators had identified as the true start of the outbreak. CONCLUSIONS: Because minimal data exists for an actual biologic attack, determining how quickly an algorithm might detect such an attack is difficult. However, application of these algorithms in combination with other data-analysis methods to historic outbreak data indicates that biosurveillance techniques for analyzing syndrome counts can rapidly detect seasonal respiratory and gastrointestinal illness outbreaks. Further research is needed to assess the value of electronic data sources for predictive detection. In addition, simulations need to be developed and implemented to better characterize the size and type of biologic attack that can be detected by current methods by challenging them under different projected operational conditions.

Algorithms↗

PubMed2004

ESSENCE II and the framework for evaluating syndromic surveillance systems.

INTRODUCTION: The Electronic Surveillance System for the Early Notification of Community-Based Epidemics (ESSENCE II) is a prototype syndromic surveillance system for capturing and analyzing public health indicators for early detection of disease outbreaks. OBJECTIVES: This paper presents a preliminary evaluation of ESSENCE II according to a CDC framework for evaluating syndromic surveillance systems. METHODS: Each major topic of the framework is addressed in this assessment of ESSENCE II performance. RESULTS: ESSENCE captures data in multiple formats, parses text strings into syndrome groupings, and applies multiple temporal and spatio-temporal outbreak-detection algorithms. During a recent DARPA evaluation exercise, ESSENCE algorithms detected a set of health events with a median delay of 1 day after the earliest possible detection opportunity. CONCLUSIONS: ESSENCE II has provided excellent performance with respect to the framework and has proven to be a useful and cost-effective approach for providing early detection of health events.

Algorithms↗

PubMed1990

Second place--Resident Clinical Science Award 1990. A porcine model of chronic endobronchial obstruction.

To elucidate the effects of both prolonged lobar atelectasis and subsequent re-expansion in a non-thoracotomized animal, we have developed a chronic, reversible porcine model of endobronchial obstruction. Eight adolescent pigs underwent the bronchoscopic placement of a left lower lobe bronchial plug. The obstruction was left in place for 24 hours. Four pigs then had the balloon bronchoscopically removed, while four controls underwent sham removal of the balloon. All animals showed significant atelectasis of the obstructed lobe compared to non-obstructed lobes at 24 hours. Pulmonary blood flow decreased significantly 24 hours after obstruction compared to pre-obstruction values in the collapsed lobe in all animals. Re-expansion was followed by arterial hypoxemia, which was accompanied by an increase in relative blood flow to the partially re-expanded lobe in the experimental group. No significant changes in lung water content occurred in the study group compared to controls.

Animals↗

PubMed1979

Unilateral pulmonary edema in rabbits after reexpansion of collapsed lung.

The effects of the mode of reinflation and of the duration of prior collapse on the development of unilateral pulmonary edema following reexpansion of collapsed lung were studied in a rabbit model simulating the human syndrome of "reexpansion pulmonary edema." The right lungs of rabbits were maintained in an atelectatic state for 0.5 h to 8 days, by injection of air into the pleural space. Reexpansion was achieved in 2 h by application of positive pressure to the airway while a chest tube was connected to underwater seal, or by application of negative pressure (-20 to -100 Torr) to a screened window in the partietal pleura. The lung surface pressures we actually applied by the two methods are not known. Animals were then killed and pulmonary edema was determined by wet-to-dry weight ratios. The incidence of unilateral pulmonary edema increased as the duration of prior collapse was increased (85% after 7--8 days; 17% after 3 days; and 0% after 0,5 h) when reinflated with -100 Torr applied to the pleural window. Although the incidence was less, it also occurred following the use of pleural window pressure less negative than -100 Torr, and after reinflation by positive airway pressure.

Airway Obstruction↗

PubMed1978

Effect of pulmonary microembolism on arteriovenous shunt flow.

The effects of acute pulmonary hypertension on the fraction of cardiac output shunted through pulmonary arteriovenous communications have been studied in dogs as a possible cause of hypoxia following pulmonary embolization. Pulmonary artery pressure was increased twofold and then fourfold above control values by embolization of the pulmonary vascular bed with polystyrene microspheres. Quantitative measurements of arteriovenous shunt were determined from the fraction of 50 mu radioactively labeled microspheres injected into the inferior vena cava which passed through the pulmonary circulation into systemic vascular beds. There was no increase in the fraction of pulmonary blood flow passing through pulmonary arteriovenous connections, 50 mu in diameter or greater, with pulmonary microembolism when FIo2 was 1. There was a small increase in arteriovenous shunt fraction when pulmonary artery pressure was increased with an FIo2 of 0.21. Physiological shunt measured by the oxygen technique did not increase with pulmonary embolism, but total venous admixture rose significantly. Postmortem gravimetric measurements of lung water indicated pulmonary edema. We conclude that anatomic arteriovenous shunt channels have little physiological significance after pulmonary microembolism in the dog lung. The major cause of hypoxia immediately after pulmonary microembolism is ventilation/perfusion imbalance, probably caused by pulmonary edema.

Animals↗