Our study demonstrates that rapid bolus administration at a rate of 999 mL/hour via either 18- or 20-gauge PIV catheter is relatively safe. Out of 216 bolus administrations of 3% HTS peripherally, complications only occurred in 8 administrations (3.7%). No severe complications, such as hypotension, osmotic demyelination, or ARDS, were identified with rapid bolus of 3% HTS via PIV catheter. Our study also demonstrated the efficacy of peripheral 3% HTS bolus to treat elevated ICP. In our study, the median ICP decreased by 4.6 mmHg (p < 0.001) after 3% HTS bolus was administered; serum sodium, chloride and serum osmolality rose as anticipated, in accordance with each bolus (p < 0.001).
There are limited studies investigating the safety of 3% HTS administration via PIV catheter. Most of the existing literature reported patients receiving 3% HTS via PIV catheter at a lower infusion rate (< 100 mL/hour) with prolonged infusion time (> 6 hours), and infusion-related complication rates ranged from 2.9–10.7%.22 One study comparing 3% HTS versus mannitol boluses via PIV catheter for neurological emergencies did not identify any bolus-related complications, but notably the authors omitted bolus rates and identified only extravasation as the sole complication of interest.21 Seven (8.2%) patients who received 3% HTS boluses also developed acute kidney injury (AKI) in the next 48 hours.21 Another study reported use of 3% HTS boluses via PIV catheter at a median rate of 760 mL/hour for neurological emergencies.16 They did not observe any adverse effects at the site of infusion, however 4 patients (12.5%) experienced hypotension while receiving the 3% HTS bolus.16 In comparison to existing literature, all patients included in our cohort received 3% HTS bolus at the rate of 999mL/hour via a 18- or 20- gauge PIV catheter for neurological emergencies and bolus-related complications occurred in 3.7% of 3% HTS bolus administrations, which aligns with the complication risk reported in the existing literature. Interestingly, the mean MAP in our cohort increased by 3.1 mmHg (p = 0.03) after 3% HTS bolus, which likely represented the volume expansion effect of 3% HTS.6
To date, our study is the largest retrospective analysis to evaluate the safety and efficacy of 3% HTS administered at a rate of 999 mL/hour peripherally, which provides valuable data to support its application in the setting of neurological emergencies. Although there were no studies that directly compared the safety or efficacy of centrally administered 3% HTS with that which is given peripherally, it is well reported in the literature that CVCs are associated with costly complications which carry morbidity and mortality risks, regardless of the infused solution.16 Our data may assuredly allow institutions to consider alteration of restrictions on administration of 3% HTS in neurological emergencies when bolus of hypertonic solution is recommended according to most recent practice guideline.1 While there is also rising interest in peripheral administration of 23.4% HTS for neurological emergencies, it is not free from serious adverse events, and most institutions still mandate the use of 23.4% HTS via CVC by slow push over 10 to 15 minutes.5 23 The use of equiosmolar dose of 3% HTS as a bolus for neurological emergencies might be a more viable alternative to 23.4% HTS when it is unavailable or unsafe to administer, but further studies directly comparing the efficacy of equiosmolar doe of 3% HTS to 23.4% HTS are warranted.
There are several inherent limitations to our study. First one is the retrospective, non-comparative, and single-center nature of its design. We relied heavily on the documentation of adverse events in the EMR, and thus it is likely that minor complications may have been underreported. However, our robust electronic safety event reporting system lends confidence that major events would be captured in review. Because this was a retrospective analysis of a hospital-wide medication administration policy change, it lacked a comparison arm. It is our institutional policy that all patients in the ICU have more than 2 PIV catheters at all times; thus, we were unable to identify exact gauge and site of PIV catheters that the 3% HTS bolus was administered through. Additionally, some PIV catheters may have had additional medications administered concomitantly with 3% HTS boluses, potentially confounding our complication analysis. We sought to include all neurologically critically ill patients, and because of their heterogenous disease processes, we lacked ICP data for every single patient. To compensate for theses missing data, we substituted it with serum electrolytes and osmolality changes following 3% HTS bolus administration, postulating that HTS decreases ICP by increasing serum osmolality and shifting extravascular fluids intravascularly.