Background: The problem of medical errors has recently received a great deal of attention, which will probably increase. In this minireview, we focus on this issue in the fields of laboratory medicine and blood transfusion.

Methods: We conducted several MEDLINE queries and searched the literature by hand. Searches were limited to the last 8 years to identify results that were not biased by obsolete technology. In addition, data on the frequency and type of preanalytical errors in our institution were collected.

Results: Our search revealed large heterogeneity in study designs and quality on this topic as well as relatively few available data and the lack of a shared definition of “laboratory error” (also referred to as “blunder”, “mistake”, “problem”, or “defect”). Despite these limitations, there was considerable concordance on the distribution of errors throughout the laboratory working process: most occurred in the pre- or postanalytical phases, whereas a minority (13–32% according to the studies) occurred in the analytical portion. The reported frequency of errors was related to how they were identified: when a careful process analysis was performed, substantially more errors were discovered than when studies relied on complaints or report of near accidents.

Conclusions: The large heterogeneity of literature on laboratory errors together with the prevalence of evidence that most errors occur in the preanalytical phase suggest the implementation of a more rigorous methodology for error detection and classification and the adoption of proper technologies for error reduction. Clinical audits should be used as a tool to detect errors caused by organizational problems outside the laboratory.

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Errors in Laboratory Medicine

The phasing out of leaded gasoline for transportation vehicles between 1973 and 1995 and the removal of lead from paint by federal mandate by 1978 have resulted in substantial lowering of mean blood lead levels in all segments of the U.S. population. However, because lead is a persistent metal, it is still present in the environment – in water, brass plumbing fixtures, soil, dust, and imported products manufactured with lead. Diagnosis of lead toxicity has traditionally been based on significantly elevated blood lead levels. However, data now implicates low-level exposures and blood lead levels previously considered normal as causative factors in cognitive dysfunction, neurobehavioral disorders, neurological damage, hypertension, and renal impairment. Chelation is the conventional recommendation in the case of blood levels associated with acute toxicity and encephalopathic damage. Issues surrounding the assessment of body lead burden and the consequences of low-level environmental exposure are critical in the treatment of chronic disease related to lead toxicity. (Altern Med Rev 2006;11(1):2-22)

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Lead Toxicity, A Review of the Literature. Part I: Exposure, Evaluation, and Treatment

/pdf/toxicological-profile-for-nickel-28n8gpgs6h.pdf

Toxicological profile for nickel

Omega-3 fatty acid supplementation accelerates chylomicron triglyceride clearance

Normal levels of trace elements in human blood plasma or serum

Ni, Cu, Zn, and Pb were measured by atomic absorption spectrometry in sweat samples obtained by the arm-bag technique from 48 healthy adult subjects (33 ♂, 15 ♀ ) during sauna bathing (15 min at 93 °C, dry heat). The men sweated more profusely than the women (volume, in milliliters, of sweat collected: mean, SD, and range: 23 ± 12 (3-55) and 7 ± 3 (2-13), respectively. The concentrations, in µg/liter, (mean, SD, and range) of trace metals in sweat of men and women, respectively, were: nickel , 52 ± 36 (7-180) and 131 ± 65 (39-270); copper , 550 ± 350 (30-1440) and 1480 ± 610 (590-2280); zinc , 500 ± 480 (130-1460) and 1250 ± 770 (530-2620); and lead , 51 ± 42 (8-184) and 118 ± 72 (49-283). In sweat samples from 11 women on oral contraceptives, concentrations of Ni, Cu, Zn, and Pb did not differ significantly from the values in the 15 control women. Sweating is a demonstrably significant route for excretion of trace metals, and sweating may play a role in trace-metal homeostasis. Essential trace metals could conceivably be depleted during prolonged exposure to heat; conversely, sauna bathing might provide a therapeutic method to increase elimination of toxic trace metals.

Atomic Absorption Spectrometry of Nickel, Copper, Zinc, and Lead in Sweat Collected from Healthy Subjects during Sauna Bathing

Background: The Laboratory Advisory System (LAS) is an expert system interface that works interactively with clinicians to assist them with test selection and result interpretation throughout the laboratory investigation of a patient.

Methods: To study the influence of the LAS on laboratory investigations, a repeated-measures experiment using clinical vignettes was conducted. To collect baseline data on how laboratory investigations are currently conducted, clinicians investigated one-half of the vignettes using a conventional (noncomputer) approach. To determine the influence of the LAS on clinicians’ behavior, the other half of the vignettes were investigated using the LAS.

Results: Clinicians using the LAS (compared with conventional practice) ordered fewer laboratory tests during the diagnostic process (mean, 17.8 vs 32.7), completed the diagnostic workup with fewer sample collections (mean, 5.8 vs 7.5), generated lower laboratory costs (mean, $194 vs $232), shortened the time required to reach a diagnosis (mean, 1 day vs 3.2 days), showed closer adherence to established clinical practice guidelines, and exhibited a more uniform and diagnostically successful investigation.

Conclusion: The LAS enhances the outcome of the investigation and improves laboratory utilization.

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The Influence of an Expert System for Test Ordering and Interpretation on Laboratory Investigations

Nickel was measured, by atomic absorption spectrometry, in serum and urine specimens from: ( a ) healthy hospital employees (age 19-62) who had resided >1 year in Sudbury, Ontario, and ( b ) healthy hospital employees (age 18-62) who had resided >1 year in Hartford, Connecticut. Subjects in groups a and b were matched according to age and sex. None of the subjects had occupational exposure to nickel. Nickel was analyzed in duplicate on a "blind" basis with specimens from groups a and b interspersed within each run. In population a , serum nickel concentrations averaged 4.6 ± 1.4 µg/liter (n = 25), urine nickel excretion 7.9 ± 3.7 µg/day (n = 19). In population b , serum nickel concentrations averaged 2.6 ± 1.0 µg/liter (n = 26), urine nickel excretion 2.5 ± 1.4 µg/ day (n = 20). These population means were all significantly different ( P <0.001, t test). Serum and urinary nickel concentrations were not significantly influenced by age or sex, nor were they correlated with length of residence in either location. Nickel concentrations in municipal tap water averaged 200 ± 43 µg/liter in Sudbury (seven sites), and 1.1 ± 0.3 µg/liter in Hartford (five sites). Measurements of nickel in serum and urine are valid biological indices of environmental exposure to nickel.

Measurements of Nickel in Serum and Urine as Indices of Environmental Exposure to Nickel

Nickel concentrations were measured by atomic absorption spectrometry in sera. The mean concentration of nickel in sera of 47 healthy adults was 2.6 SD ± 0.8) µg/liter. Abnormally high mean concentrations (µg/liter) of serum nickel were found in patients with: ( a ) acute myocardial infarction (13-36 h after onset), mean = 5.2 ± 2.8, N = 33, P 25% body surface, 37-72 h after injury), mean = 7.2, N = 3, range = 4.1-10.9. Diminished mean concentrations of serum nickel were found in patients with: ( a ) hepatic cirrhosis, mean = 1.6 ± 0.8, N = 18, P <0.005; and ( b ) chronic uremia, mean = 1.7 ± 0.7, N = 12, P = <0.005. Normal mean concentrations of serum nickel were found in patients with: ( a ) acute myocardial ischemia without infarction (13-36 h after onset), mean = 3.3 ± 1.6, N = 22; ( b ) acute trauma with fractured bones (13-36 h after injury), mean = 2.7 ± 0.9, N = 19; ( c ) acute delirium tremens (13-36 h after admission), mean = 2.3 ± 0.9, N = 25; and ( d ) muscular dystrophy, mean = 2.3 ± 1.4, N = 10. In sera collected from 12 mothers immediately after normal delivery, the mean concentration of nickel was 3.0 ± 1.2 µg/liter, the same values as for sera from the umbilical cords of their 12 full-term infants.

Abnormal Concentrations of Nickel in Serum in Cases of Myocardial Infarction, Stroke, Burns, Hepatic Cirrhosis, and Uremia

Recent investigations in our laboratory have been concerned with applications of atomic absorption spectrometry to the elucidation of nickel metabolism in health and disease.*-\" These studies have shown that nickel is maintained within characteristic ranges of concentrations in blood sera of man and several species of domestic and experimental animals:' Pathological alterations of serum nickel concentrations have been found to occur in various common diseases of man.G As summarized in TABLE 1, measurements of serum nickel are performed in our laboratory by means of a Perkin-Elmer model 403 atomic absorption spectrometer.' The addition of trichloroacetic acid (TCA) to serum dissociates nickel from serum proteins and simultaneously precipitates the proteins. Nickel is combined with pyrrolidone dithiocarbamate (PDC) , and the Ni-PDC complex is extracted into methylisobutylketone (MIBK). The MIBK extract is aspirated into the acetylene-air flame of the atomic absorption spectrometer, and absorbance is measured at 232 nm. The same technique is used for analyses of nickel in diets, excreta, and tissues, except that organic constituents are destroyed by preliminary acid digestion.', :L The sensitivity of the analytical method is 0.2 pl Ni/l of serum, expressed as the concentration of nickel that yields a recorder signal equal to twice the base line noise level. The analytical precision is 8.7%, expressed as the coefficient of variation of duplicate analyses of sera within a single run, or 9.9%, expressed as the coefficient of variation of replicate daily analyses of a single pooled serum. The mean concentration of nickel in sera from 47 healthy adults is 2.6 (S.D. 2 0.8) pg/l, with a range from 1.1-4.6 pg/l.\" TABLE 2 lists the concentrations of nickel found in sera from several species of animals.' It may be seen that there is wide variability in the mean concentrations of serum nickel in these species, but that within each species the concentrations of serum nickel fell within a relatively narrow range. The highest mean concentrations of nickel were found in sera from pigs, rabbits, and lobsters. Due to the relative abundance of nickel in rabbit serum, the rabbit has proven to be particularly well suited for studies of nickel metabolism. No significant differences were found in any of the species between the mean concentrations of nickel in sera from males and females. In man, the normal ranges of concentrations of serum nickel appear to be constant from birth to senescence and are not significantly affected by pregnancy.\" Investigations in our laboratory have confirmed the report by D'Alonzo and Pel1 7 that increased concentrations of serum nickel frequently develop within 24 hr after the onset of acute myocardial infarction. FIGURE 1 shows serial

Michael D. McNeely

Papers

Atomic Absorption Spectrometry of Nickel, Copper, Zinc, and Lead in Sweat Collected from Healthy Subjects during Sauna Bathing

The Influence of an Expert System for Test Ordering and Interpretation on Laboratory Investigations

Measurements of Nickel in Serum and Urine as Indices of Environmental Exposure to Nickel

Abnormal Concentrations of Nickel in Serum in Cases of Myocardial Infarction, Stroke, Burns, Hepatic Cirrhosis, and Uremia

Nickel metabolism in health and disease.