1. Errors arise when an action is intended but not performed; errors that arise from poor planning or inadequate knowledge are characterized as mistakes; those that arise from imperfect execution of well‐formulated plans are called slips when an erroneous act is committed and lapses when a correct act is omitted. 2. Some tasks are intrinsically prone to error. Examples are tasks that are unfamiliar to the operator or performed under pressure. Tasks that require the calculation of a dosage or dilution are especially susceptible to error. 3. The tasks of prescribing, preparation, and administration of medicines are complex, and are carried out within a complex system; errors can occur at each of many steps and the error rate for the overall process is therefore high. 4. The error rate increases when health‐care professionals are inexperienced, inattentive, rushed, distracted, fatigued, or depressed; orthopaedic surgeons and nurses may be more likely than other health‐care professionals to make medication errors. 5. Medication error rates in hospital are higher in paediatric departments and intensive care units than elsewhere. 6. Rates of medication errors may be higher in very young or very old patients. 7. Intravenous antibiotics are the drugs most commonly involved in medication errors in hospital; antiplatelet agents, diuretics, and non‐steroidal anti‐inflammatory drugs are most likely to account for ‘preventable admissions’. 8. Computers effectively reduce the rates of easily counted errors. It is not clear whether they can save lives lost through rare but dangerous errors in the medication process.

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SUMMARYObjectives: To quantify the number of doctors charged with manslaughter in the course of legitimate medical practice and to classify cases, as mistakes, slips (or lapses), and violations, using a recognized classification of human error system. That requires improvement to the complex systems of health care.

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Stepwise glucose clamps were used to study beta-cell insulin response to glucose in normal and noninsulin-dependent diabetic subjects and to study changes in response after hyperglycemia. In normal subjects, insulin increment, delta I, correlated with glucose increment above basal, delta G, during the first 6 min of hyperglycemia, r = 0.748, P less than 0.0001. After 1 h of hyperglycemia, mean delta I/ delta G was reduced from 50 to 23 (mean difference 23 +/- 5) pmol/mmol, P = 0.0002; but delta I/% change in glucose (delta G') was unaltered (2.3 vs. 1.7, mean difference 0.4 +/- 0.3 pmol/%). Second-phase response correlated with mean glucose elevation (r = 0.835, P less than 0.0001), and no plateau was reached after 3 h at 3 mmol/l above basal glucose (rate of change of insulin concentration = 0.5; range, 0.3-0.8 pmol . l-1 . min-1). In diabetic subjects, delta I/ delta G was 20% of normal, while delta I/ delta G' was 63% of normal and second-phase response 30% of normal. We conclude that hyperglycemia per se reduces delta I/ delta G and must be considered when assessing insulin responses. Noninsulin-dependent diabetic subjects have defective first- and second-phase responses.

P rescribing errors in diabetes have the potential to cause serious adverse effects. Antidiabetic agents are a significant cause of admission to hospital. Prescribing errors can be caused by poor handwriting, failure to communicate clearly, and by the use of inappropriate abbreviations. Serious errors involving insulin have been reported in the UK media. While education and training may reduce the number of errors, experience shows that errors will continue to occur without changes to systems. Br J Diabetes Vasc Dis 2009;9:84-88