We present a two-year survey of BSI in six internal medicine wards in a tertiary medical center. The BSI source could be defined in 79.4% of the POA events (67.4% secondary BSI and 12.0% CLABSI) but only in 53.8% when the BSI was hospital acquired (34.4% secondary BSI and 19.4% CLABSI). Primary non-CLABSI events were over two times more common in the HA group compared to the POA group (46.2% vs. 20.6% respectively, p=0.001) (Figure 1, Table 1).
True BSI should always warrant clinicians to look for its source, in order to treat the patient properly. In clinical practice, many times such a source cannot be defined. Several reasons can be given for that, such as lack of appropriate workup or previous antibiotic treatment. In addition, adherence to the strict CDC criteria when analyzing a BSI event can sometimes diminish the ability to classify events as secondary.
We conducted a rigorous evaluation in each BSI event in order to identify the likely source. The finding of lack of a source for HA-BSI in almost half of the cases requires explanation.
Over the last two decades, attention has been focused on central venous lines as an important and common source of BSI. The same mechanisms leading to BSI secondary to the presence of a central venous catheter (i.e. bacterial invasion through or around the catheter) (18), may apply also to PVCs. Though peripheral lines are placed for a shorter duration than central lines (19), PVCs are much more prevalent in the hospital setting. Practically, almost every hospitalized patient in the internal medicine ward has a PVC (20). These lines are usually inserted and maintained without the strict precautions applied for central lines (11). Hence, it is reasonable to conclude that PVCs can be an important source of primary non-CLABSI.
The peripheral line is an obvious cause for primary non-CLABSI when thrombophlebitis is present (13, 21–23), however in our study, thrombophlebitis was found only in 3/129 (2.3%) cases of primary non-CLABSI. Lack of local signs in primary non-CLABSI is not surprising, as patients with CLABSI also usually have no local signs of infection. We propose that when there is a BSI without a secondary cause, in the presence of a peripheral line (and without a central line), peripheral-line associated BSI (PLABSI) is the presumed diagnosis. As in the CDC guidelines for the diagnosis of CLABSI, the PLABSI definition is also not relied on tip of the line cultures (i.e. catheter-related BSI), since these are not feasible in everyday clinical practice. In our opinion, PLABSI is the commonest hospital acquired cause for primary non-CLABSI, and in most cases without local signs.
In a systematic review by Mermel (24) in most studies included, PLABSI was diagnosed by local signs of infection (i.e. thrombophlebitis). According to our findings, those events of PLABSI with local signs probably constitute only a small part of PLABSI cases.
Once the concept of PLABSI is defined, it should lead us to take appropriate preventive measures. There is plenty of information regarding CLABSI prevention, on insertion of the catheter and during its use. It is reasonable to assume that the proven practices for the prevention of CLABSI (25) can be effective as well for PLABSI prevention. (26–29). Prevention of BSI as a complication of a PVC through appropriate handling of insertion and maintenance of such lines could prevent a considerable number of deaths from HA-BSIs (30). Moreover, when there is a BSI and no secondary cause can be identified, it may be prudent to replace the peripheral line.
In our study, both in POA and HA, Gram-negative bacteria were the commonest pathogens identified followed by Staphylococcus aureus. The same prevalence was found in primary non-CLABSI (39.1% and 29.5%, respectively) (Table 4b).
We found worse outcomes of HA-BSI vs. POA-BSI, with a prolonged length of stay since the positive culture (21.4 days vs. 14.4 days, p=0.01) and significantly higher mortality rate (48.7% vs. 19.0%; OR 3.76, 95%CI, 2.46 - 5.74) (Table 1). In our cohort, the patients with HA-BSI were older and had more comorbidities compared to the patients with POA-BSI; this might explain their worse outcomes. Comparing the clinical outcomes according to the BSI source (Table 2), the mortality rates in CLABSI and primary non-CLABSI were similar and significantly higher than that in secondary BSI (43.5%, 39.7% and 25.6% respectively, p=0.001). However, in multi-variate analysis, only in CLABSI the mortality rate was significantly higher than in secondary BSI (OR 2.1, 95% CI, 1.1 to 3.8).
Our study has some limitations. We conducted analyses at the end of each month and not immediately on the date of the positive BC. This delay could have led to missing of some information. However, we conducted a thorough investigation in each case and the perspective nature of the analysis allowed us a better understanding of the disease course. Additionally, we could not record the presence of a peripheral line at the time of BSI, yet it is rare to find a patient in internal medicine wards without a line, as is known also from the literature (12). Finally, we did not prove microbiologically that the peripheral line is the cause of BSI in primary non-CLABSI. This would have been difficult to perform and was not part of this study. For the same reason, the CDC surveillance guidelines use the definition of CLABSI rather than the microbiologically proven catheter-related BSI (10).
In conclusion, we found that a large proportion (46.2%) of HA-BSI among internal medicine patients do not have a secondary cause. We suggest that the source for many of these BSIs is the peripheral line. Measures to prevent PLABSI, similar to those implemented for the prevention of CLABSI, should be applied.