The main findings of the present study were that percutaneous tracheotomy (PT) can be performed safely in aSAH patients and that consumption of analgesics, sedatives, and vasoactive drugs became markedly reduced after PT.
During the past decade, PT has become a routine method in the ICU. Randomized trials have documented a lower incidence of bleeding and infections compared with open surgical tracheotomy [5-8]. PT is cost-effective  and can be performed in a shorter procedure time than surgical tracheotomy , with minimal risk of increasing ICP . Our present finding of a median procedural time of 10 min and few adverse events corroborates these reports. Regarding cost-effectiveness, the present study did not investigate outcome or total hospital time. Nevertheless, the drastic reduction in analgesics/sedatives and vasoactive drugs observed after PT may counterbalance some or all of the cost of performing PT.
Timing of the tracheotomy in ventilated patients has been the focus of some randomized trials . One randomized controlled trial recently reported similar complication rates and patient outcomes in early versus late PT . Because the benefits of timely tracheotomy in the patient population with aSAH may differ from those in the general ICU population, it would have been of interest to perform controlled comparisons in aSAH patients or to analyze this subgroup of patients in the large randomized controlled trials that have already been performed. However, because even the biggest randomized controlled trial addressing the timing of tracheotomy included only a small number of patients with intracranial pathology, a new, prospective, randomized study in this patient population will be necessary.
Aneurysmal SAH is a life-threatening event, associated with a mortality rate as high as 75% in poor grade patients [13,14]. Some of this mortality can be attributed to delayed cerebral ischemia. Hence, optimizing the CPP (usually >70 mmHg) is a central part of the treatment protocol, and sedated patients most often require vasoactive drugs to obtain the prescribed CPP. The safety of vasoactive drugs regarding the cerebral vasculature is not well documented; therefore, titrating vasoactive drug doses as low as possible is mandatory. This is particularly important regarding the most feared complication of aSAH: cerebral vasospasm. One might raise concerns that the use of vasoactive drugs could exacerbate and/or prolong cerebral vasospasm. However, little is known about the effect of vasoactive drugs on the human intracranial vasculature. One randomized study conducted by Rondeau et al. has compared the combination of noradrenaline and dobutamine with noradrenaline alone . They hypothesized that the dobutamine-induced increase in cardiac output might reduce the incidence of intracranial vasospasm, but failed to show any difference. Experimental data in rabbits indicate that noradrenaline-induced hypertension may increase the diameter and flow in vasospastic intracranial vessels . Our clinical experience supports that noradrenaline is safe, although the benefit of high-dose noradrenaline is controversial.
Phenylephrine represents an alternative to noradrenaline and is commonly used to increase blood pressure to target CPP in neurointensive care . Dopamine is less used , but may be indicated if monotherapy with noradrenaline causes bradycardia. Adrenaline should not be used, as it may cause vasospasm . Regardless, the rate of possible vasoactive drug-induced adverse events will be lower if the target CPP can be maintained at lower levels of vasoactive drugs. The present study demonstrates that PT had a profound impact on vasoactive drug levels, with a marked and ongoing drop in drug usage during the first 3 days after PT.
Because cerebral vasospasm may lead to delayed cerebral ischemia and is a major contributor to poor outcome , prophylaxis and treatment of vasospasm are imperative. The neurointensivist will often face the dilemma between optimizing the CPP and minimizing the vasoactive and sedative/analgesic drug doses, especially if the targeted CPP must be increased further owing to documented severe vasospasm. In the present study, after PT, the CPP was easier to control; the mean ICP remained low even when the patient was less sedated. This was likely caused by the reduced level of stress associated with a PT versus an orotracheal tube.
A retrospective analysis of 312 patients in a general ICU population documented that administration of sedatives decreased after PT , while the observed decrease prior to and after tracheotomy in a 48-h perspective in a study of 1,780 patients did not reach statistical significance . Our study solely comprises aSAH patients, and the fact that these patients require ICP control may have had an impact on our findings. Many aSAH patients experience severely reduced consciousness after the ictus, and prolonged mechanical ventilation is necessary. Sedation continues during invasive ventilatory support, as guided by surveillance thresholds for ICP, CPP, blood oxygenation, and other parameters. We observed a statistically and clinically significant decrease in the consumption of sedative/analgesic drugs after PT. The doses of fentanyl and midazolam were larger than in a general ICU population , and the decrease in drug doses was greater than expected and could not be attributed to the expected natural course of disease. In contrast, the use of sedatives/analgesics was increasing during the 3 days prior to PT. At our ICU, the amount of sedatives used in aSAH patients is usually reduced as soon as is feasible; however, if such a reduction leads to ICP and/or CPP beyond the desired thresholds, sedation is again increased. Hence, tracheotomized patients experience less discomfort when their level of consciousness is increasing, compared with patients having an orotracheal tube. Both discomfort and arousal would contribute to elevations in ICP that in turn would be counteracted with increased sedative/analgesic use. This mechanism, unique for neurointensive patients, in particular those with aSAH, might explain the increasing use of sedatives/analgesics during the days prior to PT, in contrast to a general ICU population .
Our study suggests that PT is particularly well indicated in the aSAH population because it allows ICP and ABP control with much smaller amounts of sedative/analgesic drugs and opioids. This makes it difficult to detect severe vasospasm, and clinical signs are easier to monitor if the patient is awake. Documented serious vasospasm was treated with deep sedation and elevation of the CPP threshold in excess of 90 mmHg. No PTs were performed during the phase of serious cerebral vasospasm or other neurological instabilities. After PT, we observed a concomitant increase in CPP that was probably caused by the rapid decrease in sedatives/analgesics, given that there were no changes in the prescribed target CPP values. Although the increase in CPP was statistically significant, it was probably not of clinical impact.
Reduced sedation was associated with changing the ventilator mode; however, a retrospective analysis does not allow conclusions regarding this synergy. The fact that a significant number of patients went from controlled mode to spontaneous ventilation after PT was likely due to the greatly reduced opioid doses.
The present 3-month mortality rate of 25% was below the average in our general ICU population (30%) . Mortality was also low compared with previously published data [23,24], particularly considering our high fraction of patients who presented with Hunt & Hess grades 4 and 5 (“poor grade”). Mortality in this subgroup is reportedly as high as 75% [13,14]. The observation of a significantly poorer clinical grade in the patient population that underwent PT is expected, because patients with an anticipated long course of disease were more likely to be selected for PT. Aneurysmal SAH is more common in women [25,26]; correspondingly, more women underwent PT. The reason for a higher fraction of women being in a poorer clinical state prior to aneurysm repair is not obvious from the available data, but may be related to age, pre-existing co-morbidity, delays in seeking medical attention, larger hemorrhages, or possibly more problems with acute hydrocephalus.
Limitations of the study
The available observational data cannot answer the question of whether tracheotomy improved outcome or had an effect on the duration of hospitalization in this patient population. Although retrospective analyses may document associations and generate hypotheses, they cannot prove causation. A randomized trial with multifactorial analysis is necessary to investigate these aspects of PT.
Regrettably, the ICU did not register sedation and agitation scores for the patients during the entire study period. This limits our ability to interpret our findings regarding drug consumption. Likewise, GCS could not be retrieved for all days before and after PT in all patients.