Work patterns and fatigue-related risk among junior doctors

Background

To reduce fatigue‐related risk among junior doctors, recent initiatives in Europe and the USA have introduced limits on work hours. However, research in other industries has highlighted that other aspects of work patterns are important in generating fatigue, in addition to total work hours. The Australian Medical Association (AMA) has proposed a more comprehensive fatigue risk management approach.

Objectives

To evaluate the work patterns of New Zealand junior doctors based on the AMA approach, examining relationships between different aspects of work and fatigue‐related outcomes.

Methods

An anonymous questionnaire mailed to all house officers and registrars dealt with demographics, work patterns, sleepiness, fatigue‐related clinical errors, and support for coping with work demands. Each participant was assigned a total fatigue risk score combining 10 aspects of work patterns and sleep in the preceding week.

Results

The response rate was 63% (1366 questionnaires from doctors working ⩾40 hours a week). On fatigue measures, 30% of participants scored as excessively sleepy (Epworth Sleepiness Score >10), 24% reported falling asleep driving home since becoming a doctor, 66% had felt close to falling asleep at the wheel in the past 12 months, and 42% recalled a fatigue‐related clinical error in the past 6 months. Night work and schedule instability were independently associated with more fatigue measures than was total hours worked, after controlling for demographic factors, The total risk score was a significant independent risk factor for all fatigue measures, in a dose‐dependent manner (all p<0.01). Regular access to adequate supervision at work reduced the risk of fatigue on all measures.

Conclusions

To reduce fatigue‐related risk among junior doctors, account must be taken of factors in addition to total hours of work and duration of rest breaks. The AMA fatigue risk assessment model offers a useful example of a more comprehensive approach.     

Should we eradicate Helicobacter pylori infection in patients receiving nonsteroidal anti‐inflammatory drugs or low‐dose aspirin?

Whether Helicobacter pylori infection alters the risk of ulcer disease in patients receiving nonsteroidal anti‐inflammatory drugs (NSAIDs) or low‐dose aspirin is one of the most controversial topics in peptic ulcer research. This is an important management issue, particularly in countries where peptic ulcer disease is common and the prevalence of H. pylori infection is high. Current evidence shows that H. pylori infection increases the ulcer risk associated with NSAIDs or low‐dose aspirin. Eradication of H. pylori reduces the subsequent risk of endoscopic and complicated ulcers in patients who are about to start long‐term NSAIDs. Among patients with H. pylori infection and a history of ulcer bleeding who continue to use low‐dose aspirin, 1 week of eradication therapy prevents recurrent ulcer bleeding. Failure of eradication and concomitant use of NSAIDs, however, account for most cases of recurrent bleeding with low‐dose aspirin. The apparent protective effect of H. pylori in long‐term NSAIDs users reported in some studies was actually the weeding out of susceptible patients who were intolerant to NSAIDs. There is no convincing evidence that eradication of H. pylori has any clinically important adverse effect on the healing and prevention of ulcers in NSAIDs users.     

世界胃肠病学组织(WGO-OMGE)临床指南——发展中国家幽门螺杆菌感染

我非常高兴向大家推荐这份发展中国家幽门螺杆菌（H．priori）临床指南。该指南的编译是由数位在该领域具有丰富临床经验的世界知名专家共同完成的。     

The unmasking of <Emphasis Type="Italic">Pneumocystis jiroveci</Emphasis> pneumonia during reversal of immunosuppression: case reports and literature review

Background  

Pneumocystis jiroveci pneumonia (PCP) is an important opportunistic infection among immunosuppressed patients, especially in those infected with human immunodeficiency virus (HIV). The clinical presentation of PCP in immunosuppressed patients have been well-reported in the literature. However, the clinical importance of PCP manifesting in the setting of an immunorestitution disease (IRD), defined as an acute symptomatic or paradoxical deterioration of a (presumably) preexisting infection, which is temporally related to the recovery of the immune system and is due to immunopathological damage associated with the reversal of immunosuppressive processes, has received relatively little attention until recently.     

Priming of human neutrophils with N-formyl-methionyl-leucyl- phenylalanine by a calcium-independent, pertussis toxin-insensitive pathway

Resting neutrophils may be "primed" to augmented effector function, eg, superoxide (O2-) production in the respiratory burst, upon a second stimulation with a variety of soluble agonists including formylated methionyl-leucyl-phenylalanine (FMLP) and phorbol myristate acetate (PMA). At priming concentrations of FMLP (5 x 10(-9) mol/L) that did not initiate O2- generation, two metabolic activities were noted: (1) approximately a threefold increase in the baseline intracellular calcium (Ca++i) level, that was not dependent on extracellular Ca++, and (2) a rapid rise in intracellular pH that was blocked by 5-(N,N- dimethyl) amiloride (DA), that had no effect on the Ca++i response to priming. Furthermore, there were no significant increases in inositol metabolites in cells primed and stimulated with FMLP compared with cells receiving the stimulating dose of FMLP alone and pretreatment with pertussis toxin (PT) (before the addition of the priming -5 x 10(- 9) mol/L dose of FMLP), whereas abolishing the response to FMLP during the second stage of stimulation, had (1) no effect on FMLP-primed cells subsequently stimulated with PMA, and (2) only partially ablated the rise in Ca++i initiated with FMLP. That FMLP priming involved distinctive processes to those of the well characterized FMLP-coupled Ca++-dependent activation cascade was shown by the full priming effect attained in a Ca++-free buffer, which did not sustain an O2- response to a second-stage FMLP stimulation, but sustained a primed response to PMA. These data demonstrate that FMLP primes human neutrophils by a Ca++-independent and PT-insensitive pathway, offering a functional model for studying heterogeneous FMLP receptor-coupled reactions.