Risk prediction models: recalibration.
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Calibration↗
Biomedical subjects
Gareth J Parry
Publications and source records attributed to Gareth J Parry.
Assessment and optimization of mortality prediction tools for admissions to pediatric intensive care in the United kingdom.
OBJECTIVE: To assess the Pediatric Risk of Mortality (PRISM, PRISM III-12, and PRISM III-24) systems and the Pediatric Index of Mortality (PIM and PIM2) systems for use in comparing the risk-adjusted mortality of children after admission for pediatric intensive care in the United Kingdom. METHODS: All PICUs in the United Kingdom were invited to participate. Predicted probability of PICU mortality was calculated using the published algorithms for PIM, PIM2, and PRISM and compared with observed mortality. These scores, along with PRISM III-12 and PRISM III-24, whose algorithms are not published, were optimized for the United Kingdom. RESULTS: Of 26 PICUs in the United Kingdom, 22 (85%) were recruited, and sufficient prospective data were collected from 18 (69%) units on 10,197 (98%) of 10,385 admissions between March 2001 and February 2002. All published tools were found to have poor calibration but provided good discriminatory power. After estimation of UK-specific coefficients, only PIM2, PRISM III-12, and PRISM III-24 had satisfactory calibration. All models provided good discriminatory power. Funnel plots for all of the recalibrated models indicated that the risk-adjusted mortality for all units was consistent with random variation. CONCLUSIONS: PIM2, PRISM III-12, and PRISM III-24 all were found to be suitable for use in a UK PICU setting. All tools provided similar conclusions in assessing the distribution of risk-adjusted mortality in UK PICUs. It now is important that these tools be used to monitor outcome and improve the quality of pediatric intensive care within the United Kingdom.
Child↗
Neuropathies associated with excessive exposure to lead.
Exposure to lead is a ubiquitous problem of the modern era. The majority of cases of all forms of lead intoxication, especially lead neuropathy, result from industrial exposure. In the Western world meticulous monitoring in industry has reduced the risk of overt lead neuropathy. The classic form of lead neuropathy consists of weakness that primarily involves the wrist and finger extensors but which later spreads to other muscles. There is only minimal sensory involvement. Less commonly, there is a more typical toxic neuropathy with distally accentuated sensory and motor involvement. The motor neuropathy is more likely to develop following relatively short-term exposure to high lead concentrations and evolves in a subacute fashion. Prognosis for recovery is good as long as exposure is terminated promptly. The distal sensory and motor neuropathy develops after many years of exposure, evolves more slowly, and recovery is less certain. There is a generally weak relationship between the development of lead neuropathy and blood lead levels, at least for the subacute motor neuropathy, leading to speculation that the metabolic basis for the neuropathy is interference with porphyrin metabolism. Lead intoxication in humans causes axonal degeneration, but in some other species it causes a primarily demyelinating neuropathy. It should be possible to prevent lead neuropathy by good industrial hygiene. Close monitoring should identify excessive lead exposure before it causes overt neuropathy. If evidence of excessive exposure is found or if overt neuropathy develops, exposure must be terminated immediately. The role of chelation therapy in the treatment of lead neuropathy is controversial.
Animals↗
Recalibration of risk prediction models in a large multicenter cohort of admissions to adult, general critical care units in the United Kingdom.
OBJECTIVE: To assess the performance of published risk prediction models in common use in adult critical care in the United Kingdom and to recalibrate these models in a large representative database of critical care admissions. DESIGN: Prospective cohort study. SETTING: A total of 163 adult general critical care units in England, Wales, and Northern Ireland, during the period of December 1995 to August 2003. PATIENTS: A total of 231,930 admissions, of which 141,106 met inclusion criteria and had sufficient data recorded for all risk prediction models. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The published versions of the Acute Physiology and Chronic Health Evaluation (APACHE) II, APACHE II UK, APACHE III, Simplified Acute Physiology Score (SAPS) II, and Mortality Probability Models (MPM) II were evaluated for discrimination and calibration by means of a combination of appropriate statistical measures recommended by an expert steering committee. All models showed good discrimination (the c index varied from 0.803 to 0.832) but imperfect calibration. Recalibration of the models, which was performed by both the Cox method and re-estimating coefficients, led to improved discrimination and calibration, although all models still showed significant departures from perfect calibration. CONCLUSIONS: Risk prediction models developed in another country require validation and recalibration before being used to provide risk-adjusted outcomes within a new country setting. Periodic reassessment is beneficial to ensure calibration is maintained.
APACHE↗
Outcome at 6 months after admission for pediatric intensive care: a report of a national study of pediatric intensive care units in the United kingdom.
OBJECTIVE: The goal was to measure, by using the Health Utilities Index, the health status of children 6 months after admission to PICUs in the United Kingdom. METHODS: All PICUs in the United Kingdom were invited to participate. Children who were > or = 6 months of age at admission and were discharged alive from participating units during a 1-year period were eligible for this study. Children with completed consent forms who had survived to 6 months after admission received the Health Utilities Index questionnaire. RESULTS: Admission data on 7214 admissions to 22 units were collected between March 2001 and February 2002. Of those patients, 6786 survived to unit discharge, and consent for follow-up contact was obtained for 2642. At 6 months after admission, the mortality rate was estimated at 11.1% and 2034 children were still alive and contactable. Of those children, Health Utilities Index questionnaires were returned by 1455. No impairment was indicated for 767, 951, 940, 919, 962, and 939 children with respect to the Health Utilities Index sensation, cognition, emotion, pain, mobility, and self-care attributes, respectively. The mean +/- SE Health Utilities Index utility score was 0.73 +/- 0.01, with 397 children (27.3%) in full health. CONCLUSIONS: Death after pediatric intensive care in the United Kingdom is uncommon, making assessment of health status important. At 6 months after admission, there is significant morbidity. To assess the impact of strategies to improve or to optimize care on longer-term outcomes, standardized collection of data on preexisting comorbidities and illness severity is required.
Child↗
Isolated bibrachial plexopathy in a patient with type 2 diabetes.
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Brachial Plexus Neuropathies↗
Rapid resolution of quadriplegic CIDP by combined plasmapheresis and IVIg.
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Child↗
A randomised, controlled, triple-blind trial of the efficacy of homeopathic treatment for chronic fatigue syndrome.
OBJECTIVE: There is no management regime for chronic fatigue syndrome (CFS) that has been found to be universally beneficial and no treatment can be considered a "cure". Patients with CFS may use complementary and alternative medicine (CAM). Our aim was to evaluate homeopathic treatment in reducing subjective symptoms of CFS. METHOD: Using a triple-blind design (patient and homeopath blind to group assignment and data analyst blind to group until after initial analyses to reduce the possibility of bias due to data analyst), we randomly assigned patients to homeopathic medicine or identical placebo. One hundred and three patients meeting the Oxford criteria for CFS were recruited from two specialist hospital out patient departments. Patients had monthly consultations with a professional homeopath for 6 months. Main outcome measures were scores on the subscales of the Multidimensional Fatigue Inventory (MFI) and proportions of each group attaining clinically significant improvements on each subscale. Secondary outcome measures were the Fatigue Impact Scale (FIS) and the Functional Limitations Profile (FLP). Ninety-two patients completed treatment in the trial (47 homeopathic treatment, 45 placebo). Eighty-six patients returned fully or partially completed posttreatment outcome measures (41 homeopathic treatment group who completed treatment, 2 homeopathic treatment group who did not complete treatment, 38 placebo group who completed treatment, and 5 placebo group who did not complete treatment). RESULTS: Seventeen of 103 patients withdrew from treatment or were lost to follow-up. Patients in the homeopathic medicine group showed significantly more improvement on the MFI general fatigue subscale (one of the primary outcome measures) and the FLP physical subscale but not on other subscales. Although group differences were not statistically significant on four out of the five MFI subscales (the primary outcome measures), more people in the homeopathic medicine group showed clinically significant improvement. More people in the homeopathic medicine group showed clinical improvement on all primary outcomes (relative risk=2.75, P=.09). CONCLUSIONS: There is weak but equivocal evidence that the effects of homeopathic medicine are superior to placebo. Results also suggest that there may be nonspecific benefits from the homeopathic consultation. Further studies are needed to determine whether these differences hold in larger samples.
Adult↗
Symptom duration and clinical features in painful sensory neuropathy with and without nerve conduction abnormalities.
BACKGROUND: The term "small fiber sensory neuropathy" (SFSN) refers to an axonal sensory polyneuropathy predominantly affecting cutaneous sensory modalities, often associated with pain and with no evidence of large fiber involvement. We hypothesized that, in most patients, SFSN is the earliest manifestation of a nonspecific axonal neuropathy and will usually progress to involve larger, heavily myelinated sensory and motor fibers. We sought indirect evidence of this through an analysis of the correlation between symptom duration and large fiber involvement in patients with painful sensory neuropathy (PSN). METHODS: A clinical diagnosis of PSN was supported by nerve conduction studies or measurement of epidermal nerve fiber (ENF) density in 43 patients. Symptom duration was correlated with the frequency of large fiber loss as measured by nerve conduction abnormalities. The severity and extent of clinical signs and symptoms were also evaluated in subjects with and without electrodiagnostic abnormalities. RESULTS: Patients with large sensory axon involvement had symptoms of longer duration than patients with SFSN. The frequency of electrodiagnostic abnormalities increased in direct proportion to disease duration. Patients with electrodiagnostic abnormalities also had more extensive pinprick sensory deficits, suggesting that small fiber loss was more advanced in this group as well. CONCLUSIONS: In PSN, the incidence of large fiber involvement appears to increase in proportion to symptom duration. This represents indirect evidence that SFSN usually progresses to involve both large and small fibers within 2-10 years.
Adult↗
Static magnetic field therapy for symptomatic diabetic neuropathy: a randomized, double-blind, placebo-controlled trial.
OBJECTIVE: To determine if constant wearing of multipolar, static magnetic (450G) shoe insoles can reduce neuropathic pain and quality of life (QOL) scores in symptomatic diabetic peripheral neuropathy (DPN). DESIGN: Randomized, placebo-control, parallel study. SETTING: Forty-eight centers in 27 states. PARTICIPANTS: Three hundred seventy-five subjects with DPN stage II or III were randomly assigned to wear constantly magnetized insoles for 4 months; the placebo group wore similar, unmagnetized device. INTERVENTION: Nerve conduction and/or quantified sensory testing were performed serially. MAIN OUTCOME MEASURES: Daily visual analog scale scores for numbness or tingling and burning and QOL issues were tabulated over 4 months. Secondary measures included nerve conduction changes, role of placebo, and safety issues. Analysis of variance (ANOVA), analysis of covariance (ANCOVA), and chi-square analysis were performed. RESULTS: There were statistically significant reductions during the third and fourth months in burning (mean change for magnet treatment, -12%; for sham, -3%; P<.05, ANCOVA), numbness and tingling (magnet, -10%; sham, +1%; P<.05, ANCOVA), and exercise-induced foot pain (magnet, -12%; sham, -4%; P<.05, ANCOVA). For a subset of patients with baseline severe pain, statistically significant reductions occurred from baseline through the fourth month in numbness and tingling (magnet, -32%; sham, -14%; P<.01, ANOVA) and foot pain (magnet, -41%; sham, -21%; P<.01, ANOVA). CONCLUSIONS: Static magnetic fields can penetrate up to 20mm and appear to target the ectopic firing nociceptors in the epidermis and dermis. Analgesic benefits were achieved over time.
Adult↗
Sensory-predominant, painful, idiopathic neuropathy: inflammatory changes in sural nerves.
Sensory-predominant, painful, idiopathic neuropathies are a common clinical problem. In this retrospective study of 11 patients with such a neuropathy, we found axonal loss in 9, with multifocal axonal loss in 4 patients; there were large perivascular mononuclear inflammatory infiltrates (>50 cells) in 4 and smaller infiltrates (10-20 cells) in 4. These findings suggest that some cases of this neuropathy may be due to autoimmune vasculopathy and therefore may respond to immunotherapy.
Adult↗
Randomized, controlled trial of intravenous immunoglobulin in myasthenia gravis.
We initiated a randomized, double-blinded, placebo-controlled trial of intravenous immunoglobulin (IVIG) treatment in myasthenia gravis (MG). Patients received IVIG 2 gm/kg at induction and 1 gm/kg after 3 weeks vs. 5% albumin placebo. The primary efficacy measurement was the change in the quantitative MG Score (QMG) at day 42. Fifteen patients were enrolled (6 to IVIG; 9 to placebo) before the study was terminated because of insufficient IVIG inventories. At day 42, there was no significant difference in primary or secondary outcome measurements between the two groups. In a subsequent 6-week open-label study of IVIG, positive trends were observed.
Adult↗
Force assessment in periodic paralysis after electrical muscle stimulation.
OBJECTIVE: To obtain an objective measure of muscle force in periodic paralysis, we studied ankle dorsiflexion torque during induced paralytic attacks in hyperkalemic and hypokalemic patients. SUBJECTS, PATIENTS, AND METHODS: Dorsiflexor torque after peroneal nerve stimulation was recorded during provocative tests on 5 patients with hypokalemic or hyperkalemic disorders and on 2 control subjects (1995-2001). Manual strength assessment was simultaneously performed in a blinded fashion. Standardized provocation procedures were used. RESULTS: The loss of torque in hyperkalemic patients roughly paralleled the loss of clinically detectable strength, whereas in the hypokalemic patients, pronounced torque loss occurred well before observed clinical effects. No dramatic changes occurred in the control subjects. Torque amplitude decreased more than 70% in all patients during the provocation tests; such decreases were associated with alterations induced in serum potassium concentrations. CONCLUSIONS: Stimulated torque measurement offers several advantages in characterizing muscle dysfunction in periodic paralysis: (1) it is independent of patient effort; (2) it can show a definitely abnormal response early during provocative maneuvers; and (3) characteristics of muscle contraction can be measured that are unobservable during voluntary contraction. Stimulated torque measurements can characterize phenotypic muscle function in neuromuscular diseases.
Adolescent↗
Diabetic neuropathy.
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Diabetic Angiopathies↗