Joep M. Droogh

Quality of interhospital transport of the critically ill: impact of a Mobile Intensive Care Unit with a specialized retrieval team.

IntroductionIn order to minimize the additional risk of interhospital transport of critically ill patients, we started a mobile intensive care unit (MICU) with a specialized retrieval team, reaching out from our university hospital-based intensive care unit to our adherence region in March 2009. To evaluate the effects of this implementation, we performed a prospective audit comparing adverse events and patient stability during MICU transfers with our previous data on transfers performed by standard ambulance.MethodsAll transfers performed by MICU from March 2009 until December 2009 were included. Data on 14 vital variables were collected at the moment of departure, arrival and 24 hours after admission. Variables before and after transfer were compared using the paired-sample T-test. Major deterioration was expressed as a variable beyond a predefined critical threshold and was analyzed using the McNemar test and the Wilcoxon Signed Ranks test. Results were compared to the data of our previous prospective study on interhospital transfer performed by ambulance.ResultsA total of 74 interhospital transfers of ICU patients over a 10-month period were evaluated. An increase of total number of variables beyond critical threshold at arrival, indicating a worsening of condition, was found in 38 percent of patients. Thirty-two percent exhibited a decrease of one or more variables beyond critical threshold and 30% showed no difference. There was no correlation between patient status at arrival and the duration of transfer or severity of disease. ICU mortality was 28%. Systolic blood pressure, glucose and haemoglobin were significantly different at arrival compared to departure, although significant values for major deterioration were never reached. Compared to standard ambulance transfers of ICU patients, there were less adverse events: 12.5% vs. 34%, which in the current study were merely caused by technical (and not medical) problems. Although mean Acute Physiology and Chronic Health Evaluation II (APACHE II) score was significantly higher, patients transferred by MICU showed less deterioration in pulmonary parameters during transfer than patients transferred by standard ambulance.ConclusionsTransfer by MICU imposes less risk to critically ill patients compared to transfer performed by standard ambulance and has, therefore, resulted in an improved quality of interhospital transport of ICU patients in the north-eastern part of the Netherlands.

Antihypertensive and antihypertrophic effects of omapatrilat in SHR

Vasopeptidase inhibitors, such as omapatrilat are single molecules that simultaneously inhibit neutral endopeptidase (NEP) and angiotensin converting enzyme (ACE). In normotensive rats, a single dose of oral omapatrilat (10 mg/kg) and 1 mg/kg inhibited plasma ACE (P < .01) for 24 h and increased plasma renin activity for 8 h (P < .01). In vitro autoradiography using the specific NEP inhibitor radioligand 125I-RB104 and the specific ACE inhibitor radioligand 125I-MK351A showed omapatrilat (10 mg/kg) caused rapid and potent inhibition of renal NEP and ACE, respectively, for 24 h (P < .01). In spontaneously hypertensive rats, 10 days of oral omapatrilat (40 mg/kg/day) reduced blood pressure (vehicle 237 +/- 4 mm Hg; omapatrilat, 10 mg/kg, 212 +/- 4 mm Hg; omapatrilat 40 mg/kg, 197 +/- 4 mm Hg, P < .01) in a dose-dependent manner (10 v 40 mg/kg, P < .01). Left ventricular hypertrophy was significantly reduced by high-dose omapatrilat (vehicle 2.76 +/- 0.03 mg/g body weight; omapatrilat, 10 mg/kg, 2.71 +/- 0.02 mg/g; omapatrilat 40 mg/kg, 2.55 +/- 0.02 mg/g, P < .01) and omapatrilat also increased kidney weight compared to vehicle (both doses, P < .01). Omapatrilat caused significant inhibition of plasma ACE and increased plasma renin activity (both doses, P < .01), and in vitro autoradiographic studies indicated sustained inhibition of renal ACE and NEP (both doses, P < .01). Omapatrilat is a potent vasopeptidase inhibitor, and its antihypertensive effects are associated with inhibition of NEP and ACE at the tissue level and beneficial effects on cardiovascular structure. Relating the degree of tissue inhibition to physiologic responses may allow further definition of the role of local renin angiotensin and natriuretic peptide systems in the beneficial effects of vasopeptidase inhibitors.

Inter-hospital transport of critically ill patients; expect surprises

IntroductionInter-hospital transport of critically ill patients is increasing. When performed by specialized retrieval teams there are less adverse events compared to transport by ambulance. These transports are performed with technical equipment also used in an Intensive Care Unit (ICU). As a consequence technical problems may arise and have to be dealt with on the road. In this study, all technical problems encountered while transporting patients with our mobile intensive care unit service (MICU) were evaluated.MethodsFrom March 2009 until August 2011 all transports were reviewed for technical problems. The cause, solution and, where relevant, its influence on protocol were stated.ResultsIn this period of 30 months, 353 patients were transported. In total 55 technical problems were encountered. We provide examples of how they influenced transport and how they may be resolved.ConclusionThe use of technical equipment is part of intensive care medicine. Wherever this kind of equipment is used, technical problems will occur. During inter-hospital transports, without extra personnel or technical assistance, the transport team is dependent on its own ability to resolve these problems. Therefore, we emphasize the importance of having some technical understanding of the equipment used and the importance of training to anticipate, prevent and resolve technical problems. Being an outstanding intensivist on the ICU does not necessarily mean being qualified for transporting the critically ill as well. Although these are lessons derived from inter-hospital transport, they may also apply to intra-hospital transport.

Transferring the critically ill patient: are we there yet?

During the past few decades the numbers of ICUs and beds has increased significantly, but so too has the demand for intensive care. Currently large, and increasing, numbers of critically ill patients require transfer between critical care units. Inter-unit transfer poses significant risks to critically ill patients, particularly those requiring multiple organ support. While the safety and quality of inter-unit and hospital transfers appear to have improved over the years, the effectiveness of specific measures to improve safety have not been confirmed by randomized controlled trials. It is generally accepted that critically ill patients should be transferred by specialized retrieval teams, but the composition, training and assessment of these teams is still a matter of debate. Since it is likely that the numbers and complexity of these transfers will increase in the near future, further studies are warranted.

Bedside lung ultrasound in the critically ill patient with pulmonary pathology: different diagnoses with comparable chest X-ray opacification

The differential diagnosis and treatment of opacifications on the chest X-ray in critically ill patients may be challenging. This holds in particular the patient that suffers from respiratory failure with hemodynamic instability. Opacification in the chest X-ray could be the result of hematothorax, pleural effusion, atelectasis, or consolidation. Physical examination of such patients may not always indicate what the cause of the opacification is and thus may not always help indicate the correct therapeutic approach. In such cases, bedside ultrasound may be very helpful. We present two cases with similar chest X-ray opacifications but different diagnoses established with the help of a bedside lung ultrasound. There is documented accuracy of ultrasound in differentiating pleural effusions from consolidation. Ultrasound is safe and may be an alternative for computed tomography scan in a hemodynamically or respiratory unstable intensive care patient.

A prolonged ICU stay after interhospital transport

Transport of critically ill patients can be complicated [1-3]. Barratt and colleagues studied patients transferred for nonclinical reasons to evaluate the consequences of transportation [4]. Th ere was no diff erence in mortality but the ICU length of stay (LOS) increased by 3 days, which was explained as a negative impact of the transport on patient physiology. We disagree with this conclusion. First, by including only transports to level 3 ICUs the received level of care for transported patients will increase, introducing a bias. Second, the increase in LOS can be interpreted as a result of selection bias, because patients with a short expected LOS would often not be considered eligible for transport. Also, since there was no increase in mortality, which would have been expected with an increased LOS, we might be looking at a mortality reduction as a result of the transfer to a higher-level ICU. Th ird, Barrett and colleagues suggest that deterioration of patient physiology during transport is probably respon sible for the increase in LOS. However, the reported Intensive Care National Audit and Research Centre scores before and after transport (although not validated for sequential patient assessments) do not support this assumption. Fourth, the method of transportation should have been included in this study. Specialised transport teams deliver patients with a better acute physiology compared with nonspecialised teams [2,5], making a need for regaining physiological stability unlikely. In conclusion, we congratulate Barratt and colleagues for their research. However, we think their conclusion is premature because multiple possible confounders were not taken into account.

You do something to me, something deep inside

The use of left ventricular assist devices (LVAD) in a much broader population has led to a linear increase in implantation rates in the last decade.1 Due to improvements in technology and better care, survival rates increased significantly, but thromboembolic stroke remains a feared complication in patients assisted by an LVAD. A vast majority of these strokes occur despite adequate anticoagulation and even with the new magnetically levitated devices, stroke rates are still high.2 It is currently insufficiently clear how stroke can be prevented in these patients as no phase III clinical trials on anticoagulation in patients with LVADs have been performed. A systematic review on the relation between anticoagulation protocols and occurrence of stroke after LVAD implantation found that platelet aggregation inhibitors are the most important in preventing thromboembolic stroke and should be part of the anticoagulation protocol.3 Antiplatelet therapy might even be sufficient without the addition of coumarins, but this should be supported by a qualitative assessment of the coagulation status such as thromboelastometry and platelet function assays besides the classical parameters [i.e. international normalized ratio (INR), activated partial thromboplastin time (aPTT), and platelet count]. With such information, it would be possible to calibrate the antithrombotic therapy, deciding dose variation or withdrawal of either anticoagulant or antiaggregant therapy, on a mechanistic basis. On the other hand, the most routinely used antiplatelet, acetylsalicylic acid, had limited ability to prevent shear stress-mediated platelet activation (SMPA) for platelets subjected to elevated shear via cyclic passage through a continuous-flow ventricular assist device operating under normal clinical conditions (speed, flow rate).4 Although these were in vitro experiments and purified platelets instead of whole blood were used, it may indicate that combinational drug strategies or new

Arterial blood pressure changes induced by acceleration during mobile intensive care unit patient transport are not patient related: beware of misinterpretation

Dear Editor, Critically ill patients are transferred more safely with a mobile intensive care unit (MICU) and specialised retrieval team [1, 2], although incidents still occur [3]. However, transports are becoming more challenging [4]. During MICU transports, we repeatedly observed arterial blood pressure variations, concurrent with ambulance accelerations and decelerations. We aimed to evaluate whether the observed influence of acceleration on blood pressure is a real blood pressure change or a physical measurement artefact. Usually, the pressure transducer is positioned at the rear end of the trolley and the distance to the arterial cannula varies between 100 and 150 cm. In an experimental setting, pressure lines (Edwards Lifesciences, Irvine, USA) were positioned on the trolley. At the site of normal catheter insertion, the line was connected to a pressurised bag to simulate a static mean arterial pressure (MAP). The length of the pressure line and the baseline pressure were varied (0, 50, 100, 150 cm and 50, 75, 100 mmHg). To simulate acceleration and deceleration the trolley was moved forward and backward in several test runs. Pressures and accelerations (accelerometer, University of Twente, Enschede, the Netherlands) were measured for the different pressures and different pressure line lengths. Pressure data were plotted against acceleration data (Fig. 1). The Pearson’s correlation coefficients r, p values, R and the slopes of the linear regression lines (b) and their 95 % confidence intervals are listed in Table 1. In this experimental setting both an increase in the baseline pressure and in pressure line length were associated with significant increases in pressure variations during accelerations. To confirm the findings that pressure variations may be a physical phenomenon, MAP and acceleration data were collected during six transports. The medical ethics committee approved this study and the need for consent was waived. The pressure transducer was initially positioned at the rear end of the trolley and halfway changed to directly on top of the arterial cannula so that patients served as their own control. The effect of acceleration on MAP was analysed for both positions of the transducer. In patient transfers, a weak correlation was observed between acceleration and blood pressure with the transducer positioned on top of the arterial cannula. The mean Pearson’s r significantly increased from 0.09 to 0.50 when the transducer changed position to the rear end of the trolley. The inertial mass effect of the fluid column in the tubing explains most of the blood pressure variation. The