Clinical incidents examples

Reporting and learning systems 83 Table 5.2 Examples of designated clinical incidents to be reported... 

Bacterial resistance to antibiotics has been recognized since the first drugs were introduced for clinical use. The sulphonamides were introduced in 1935 and approximately 10 years later 20% of clinical isolates of Neisseria gonorrhoeae had become resistant. Similar increases in sulphonamide resistance were found in streptococci, coliforms and other bacteria. Penicillin was first used in 1941, when less than 1 % of Staphylococcus aureus strains were resistant to its action. By 1947,3 8% of hospital strains had acquired resistance and currently over 90% of Staph, aureus isolates are resistant to penicillin. Increasing resistance to antibiotics is a consequence of selective pressure, but the actual incidence of resistance varies between different bacterial species. For example, ampicillin resistance inEscherichia coli, presumably under similar selective pressure as Staph, aureus with penicillin, has remained at a level of 30-40% for mai years with a slow rate of increase. Streptococcus pyogenes, another major pathogen, has remained susceptible to penicillin since its introduction, with no reports of resistance in the scientific literature. Equally, it is well recognized that certain bacteria are unaffected by specific antibiotics. In other words, these bacteria have always been antibiotic-resistant. 

Also, we have noted that patients with unilateral cataracts after trauma or retinal detachment repair typically have very similar RRS carotenoid levels in the normal and in the pseudophakic eye. Thus, we have concluded that there is a decline of macular carotenoids that reaches a low steady state just at the time when the incidence and prevalence of AMD begins to rise dramatically. While this age effect has been noticed sometimes also in other studies using clinical populations and different MP detection methods (Sharifzadeh et al. 2006, Nolan et al. 2007), several groups have reported constant, age-independent MP levels. Examples include reflectance-based population studies in which respective average MP optical densities of 0.23 (Delori et al. 2001), 0.33 (Berendschot et al. 2002), and 0.48 (Berendschot and Van Norren 2004) were determined. 

For less well defined incidents however, these detection systems may be inadequate. Portable chemical detectors may not be able to be deployed to the site, not detect the agen, or give inconclusive results. Clinical findings may be non-specific, present in an atypical manner, or for example in the case of sulphur mustard, have a latency period that delays firm pattern recognition. Due to the physico-chemical properties of the agent or the time between release and collection, environmental samples may have low agent levels or sufficiently high contaminants to prevent adequate results. 

While profound immunosuppression can lead to an increased incidence of infectious or neoplastic diseases, interpreting data from experimental immunotoxicology studies or epidemiological studies for quantitative risk assessment purposes can be problematic. This is because inadvertent exposures to immunotoxic agents may often be expressed as a mild-to-moderate change, reflected, for example, by a 15 to 25% decrement in an immune parameter compared to control values. To help address the clinical consequences of mild-to-moderate immunosuppression, we examined available experimental, clinical and epidemiological studies that examined the association between suppression of immune function and infectious disease, independent of the etiology of suppression. 

---