Pain management in trauma patients in (pre)hospital based emergency care: current practice versus new guideline.

INTRODUCTION: Acute pain in trauma patients in emergency care is still undertreated. Early pain treatment is assumed to effectively reduce pain in patients and improve long-term outcomes. In order to improve pain management in the chain of emergency care, a national evidence-based guideline was developed. The aim of this study was to assess whether current practice is in compliance with the guideline 'Pain management for trauma patients in the chain of emergency care' from the Netherlands Association for Emergency Nurses (in Dutch NVSHV), and to evaluate early and initial pain management for adult trauma patients in emergency care. METHODS: Chart reviews were conducted in three regions of the Netherlands using electronic patient files of trauma patients from the chain of emergency care. We included one after-hours General Practitioner Co-operation (GPC), one ambulance Emergency Medical Services (EMS), two Helicopter Emergency Medical Services (HEMS), and three Emergency Departments (EDs). Organisation of pain management, pain assessment, and pain treatment was examined and compared with national guideline recommendations, including quality indicators. RESULTS: We assessed a random sample of 1066 electronic patient files. The use of standardised tools to assess pain was registered in zero to 52% of the electronic patient files per organisation. Registration of (non-)pharmacological pain treatment was found in less than half of the files. According to the files, pharmacological pain treatment deviated from the guideline in 73-99% of the files. Time of administration of medication was missing in 73-100%. Reassessment of pain following pain medication was recorded in half of the files by the HEMS, but not in files of the other organisations. CONCLUSIONS: The (registration of) current pain management in trauma patients in the chain of emergency care varies widely between healthcare organisation, and deviates from national guideline recommendations. Although guideline compliance differs across groups of healthcare professionals, maximum compliance rate with indicators registered is 52%. In order to improve pain management and evaluate its effectiveness, we recommend to improve pain registration in patient files. Furthermore, we advise to identify barriers and facilitators related to the implementation of the national guideline in all emergency care organisations.

Effects of physician-based emergency medical service dispatch in severe traumatic brain injury on prehospital run time.

INTRODUCTION: Prehospital care by physician-based helicopter emergency medical services (P-HEMS) may prolong total prehospital run time. This has raised an issue of debate about the benefits of these services in traumatic brain injury (TBI). We therefore investigated the effects of P-HEMS dispatch on prehospital run time and outcome in severe TBI. METHODS: Prehospital run times of 497 patients with severe TBI who were solely treated by a paramedic EMS (n = 125) or an EMS/P-HEMS combination (n = 372) were retrospectively analyzed. Other study parameters included the injury severity score (ISS), Glasgow Coma Scale (GCS), prehospital endotracheal intubation and predicted and observed outcome rates. RESULTS: Patients who received P-HEMS care were younger and had higher ISS values than solely EMS-treated patients (10%; P = 0.04). The overall prehospital run time was 74 ± 54 min, with similar out-of-hospital times for EMS and P-HEMS treated patients. Prehospital endotracheal intubation was more frequently performed in the P-HEMS group (88%) than in the EMS group (35%; P<0.001). The prehospital run time for intubated patients was similar for P-HEMS (66 (51-80)min) and EMS-treated patients (59 (41-88 min). Unexpectedly, mortality probability scores and observed outcome scores were less favourable for EMS-treated patients when compared to patients treated by P-HEMS. CONCLUSION: P-HEMS dispatch does not increase prehospital run times in severe TBI, while it assures prehospital intubation of TBI patients by a well-trained physician. Our data however suggest that a subgroup of the most severely injured patients received prehospital care by an EMS, while international guidelines recommend advanced life support by a physician-based EMS in these cases.

Rate of the myogenic response increases with the constriction level in rabbit femoral arteries.

The myogenic response forms an important aspect of blood flow regulation and is usually quantified by the steady-state relation between pressure and diameter. The aim of the present study is to analyze the dynamics of the myogenic response. In six isolated rabbit femoral arteries, the time course of the active part of the diameter response to a pressure step from 95 to 110 cm H2O (from 9.5 to 11 kPa), at two levels of norepinephrine (NE)-induced constriction, was fitted to a monoexponential curve to obtain the time constant. The NE concentrations used in the superfusion solution were between 0.8 and 1.5 microM for high constriction and between 0.2 and 0.6 microM for low constriction. Acetylcholine (1 microM in perfusion) was used to check endothelial function. The respective median values of the time constants with and without endothelium, are 13.2 and 15.5 sec (NS) for the high level of constriction and 49.5 and 58.5 sec (NS) for the low constriction level. Time constants at the two constriction levels were significantly different (p = 0.002). In seven separate experiments using 40 mM KCl, in the superfusion fluid, to constrict femoral arteries to the same level as during the high level of NE constriction, it was found that the amplitude of the myogenic response was much smaller, compared with the norepinephrine experiments, and the time constant was significantly longer (median: 80.8 sec). We conclude that the dynamics of the myogenic response in the rabbit femoral artery is independent of the endothelium, but is dependent on the constriction level and type of constricting agent.

Atracurium induced vasodilatation is not mediated by histamine in the isolated femoral artery of the rabbit.

Atracurium causes a decrease in systemic vascular resistance (SVR) and mean arterial blood pressure (MAP) which has been ascribed to histamine release. However, histamine receptor blockade does not prevent these decreases completely. The hypotensive side effects of atracurium may not only be caused by histamine. In this study we examined the vasoactive effects of atracurium with and without histamine receptor blockade in an isolated femoral artery preparation of the rabbit. We also investigated whether vasodilatation caused by atracurium depends on the presence of endothelial cells. Tyrode perfused, rabbit femoral arteries were constricted with noradrenaline (NA) to +/- 70% of their passive diameter. Endothelial function was checked with acetylcholine (ACh). The vessels were divided into two groups. In both groups the responses to histamine (1.0-10(-6)M) and atracurium (3.2-10(-5)M) were determined. In group one (n = 5), the histamine and atracurium responses were repeated during histamine receptor blockade. In group two (n = 5), the diameter responses to histamine and atracurium before and after endothelium removal were compared. Also, some vessel segments (n = 5) were histologically prepared and examined for mast cells. The vasodilatory responses to atracurium both with and without histamine receptor blockade were the same. Removal of endothelium caused an increase in the histamine response, while the dilating response to atracurium remained constant. We conclude that in the isolated femoral artery of the rabbit, atracurium induces, vasodilatation that is not mediated by histamine release and cannot be prevented with histamine receptor blockade. The mechanism of atracurium induced dilation is independent of the endothelium and is located in the smooth muscle cell.

Intraluminal pressure modulates the magnitude and the frequency of induced vasomotion in rat arteries.

Arterial vasomotion and its relation to intraluminal pressure were investigated in vitro in isolated rat arteries. Femoral arteries (mean diameter = 768.2 +/- 25 microns, n = 5) and mesenteric arteries (mean diameter = 393.4 +/- 32 microns, n = 5) were used in this study. Arterial segments were excised, mounted on microcannulas and perfused with Tyrode's solution at a constant flow (100 microliters/min). After equilibration, intraluminal pressure was stepwise changed from 0 to 120 mm Hg. The changes in the outer diameter of the vessels were measured continuously over a period of 4 h after the equilibration. Vasomotion was induced by constrictor agonists (norepinephrine 10(-6) M for mesenteric arteries and norepinephrine 10(-6) M + Bay K8644 10(-7) M for femoral arteries) and was maintained only in the presence of the above-mentioned drugs. Both vasomotion magnitude and frequency are modulated by pressure. Vasomotion frequency increases with pressure increase. When intraluminal pressure varied between 0 and 120 mm Hg, vasomotion frequency varied between 0.19 and 0.49 Hz for mesenteric arteries and between 0.04 and 0.23 Hz for femoral arteries. Thus, vasomotion frequency differed clearly between the two vessel types. Vasomotion amplitude shows a biphasic relationship with a maximum occurring at about 40 mm Hg for mesenteric arteries and 50 mm Hg for femoral arteries. Based on these findings, it is hypothesized that vasomotion amplitude relates to the active mechanical properties of the artery and, in particular, to its contractile capacity.

Endothelium function is protected by albumin and flow-induced constriction is independent of endothelium and tone in isolated rabbit femoral artery.

To investigate the preservation of endothelial function, we perfused two segments of one rabbit femoral artery (n = 8) in a pressure myograph in parallel, both with Tyrode, but one with 0.6% albumin added. The change in the outer diameter of the vessels [preconstricted with norepinephrine (NE) to 70%] in response to acetylcholine as an indicator of the endothelial function, was repeatedly measured over 5 h after the equilibration. The difference between the acetylcholine responses of the two vessel segments was significant (p < 0.05) after a perfusion period of 4 h. We also investigated whether flow-induced constriction is dependent on (1) the presence of endothelium and (2) the level of preconstriction. We therefore perfused segments of rabbit femoral arteries (n = 5) with Tyrode with 0.6% albumin. If acetylcholine-induced dilatation was present, a flow-diameter relation was determined at two constriction levels: about 60% (high) and 90% (low) of the passive outer diameter. Both determinations were repeated after mechanical endothelium removal (checked functionally and histologically). A similar decrease in diameter (about 7%) with an increase in flow ranging from 0 to 1,330 microliters/min was found in all conditions. We conclude that the addition of (0.6%) albumin protects endothelial function in the rabbit femoral artery when perfused in the low-flow range for a period longer than 4 h. We also found that flow-dependent constriction is neither influenced by the presence of the endothelium nor by the level of tone induced with NE.

A new mounting technique for perfusion of isolated small arteries: the effects of flow and oxygen on diameter.

There is at present no suitable technique available for performing pressure-flow studies in isolated small arteries (i.e., less than 500 microns), in which the effects of flow and pressure on artery dimensions can be studied independently. A new mounting technique is presented in which the ends of a vessel segment are cemented to the inner surface of two cannulae, with a tip diameter slightly larger than the outer diameter of the vessel, using two-component human fibrin glue. By means of this technique the pressure drop over the cannulae can be made small. First the effect of the glue on constrictive properties is studied. The glue used has no significant influence on the norepinephrine dose-response relation or on the relaxation in response to 1.0 microM acetylcholine. Small mesenteric arteries of the rabbit with outer passive diameters (at zero pressure) of 315 microns (+/- 22 microns SEM) are studied with this method. The effects of flow (shear stress) and oxygen are investigated (vessels are preconstricted (30%) with norepinephrine (1-2 microM)). The flow range used resulted in shear stresses between 0 and 290 dyn.cm-2, a range including values found in vivo. There is a significant (P less than 0.001) decrease in diameter when flow is increased, and hypoxia (pO2 less than 30 mm Hg) augmented the preconstriction with norepinephrine (P = 0.002). The flow effect and the oxygen influence are independent of each other. These results are similar to our previous findings in the femoral artery of the rabbit (diameter about 1200 microns).

Arteriolar and venular reactivity to superfusate pO2 in tissues with different metabolic capacity. A study in skeletal muscle and mesentery of the rat.

In skeletal muscle (extensor hallucis proprius) and mesentery of anesthetised (pentobarbital 30 mg/kg) female rats (200 g) we have compared reactivity to O2 of arterioles and venules with their response to a vasoconstrictor (epinephrine 5.5 x 10(-7) M) and a vasodilator (adenosine 10(-4) M). Muscle arterioles fully constricted with O2 and epinephrine and dilated with adenosine (22%). Muscle venules did not respond to changes in superfusate pO2, constricted 18% with epinephrine and dilated 10% with adenosine. In the mesentery changes in superfusate pO2 had no effect on diameters of arterioles or venules but epinephrine fully constricted arterioles and constricted venules by 19%, while adenosine dilated arterioles (6%) but not venules. When we set arteriolar and venular diameters during adenosine superfusion at 100%, muscle arterioles appeared to operate at 63% and mesenterial arterioles at 84% of maximal diameter at normal tissue pO2. For venules these percentages were 91 and 97%, respectively. Arterioles and venules in muscle thus have higher tone and muscle arterioles are greatly sensitive to changes in tissue pO2 while in our preparation mesenterial arterioles are not.

Effects of oxygen and flow on the diameter of the femoral artery of the rabbit.

Contradictory results concerning the effects of oxygen and flow on blood vessel dimensions have been published. The aim of this study was to investigate the diameter changes in isolated, cannulated femoral arteries (n = 5) of the rabbit in a preconstricted state (two norepinephrine levels) during high and low pO2 (both inside and outside) at different flow levels. In this way the interaction between oxygen and flow is also investigated. Results were normalized to relative diameters, where the diameter at zero flow, during high pO2 and low norepinephrine concentration was considered as a control diameter (100%). We found three effects in this study: (1) going from high to low oxygen, there was a global vasoconstriction (repeated measures, analysis of variance, p = 0.016 with low norepinephrine and p = 0.015 with high norepinephrine); (2) when flow was increased from 1 to 100 ml/h, we found a significant (p less than 0.001) flow-dependent constriction under all four conditions, and (3) there is an interaction between flow and oxygen, for example at low norepinephrine the constriction due to low oxygen is 16% at zero flow and 1% at a flow of 1 ml/h, at high norepinephrine these numbers are 22 and 10%, respectively.

Does the endothelium play a role in flow-dependent constriction? A study in the isolated rabbit femoral artery.

We studied the role of the endothelium in diameter changes as a function of flow of the isolated femoral artery of the rabbit (n = 15) perfused and superfused with a physiological salt solution (37 degrees C). In 10 vessels, diameters were studied before and after exposure to gossypol, an agent that impairs the endothelial function pharmacologically. In 5 of these 10 vessels we added albumin (1.5%) to the perfusion solution. The mean external diameter (+/- SEM) after equilibration for 60 min at a transmural pressure of 50 cm H2O (n = 10) was: 1,426 +/- 34 microns. Vessels were then constricted with norepinephrine (1.0-1.5 microM in the superfusion solution) to 70% of the resting diameter, acetylcholine was used to check endothelial function. All vessels constricted as flow was increased (p less than 0.001), irrespective of the impairment of the endothelial function by gossypol or the presence of albumin. It is therefore unlikely that the flow-induced constriction results from a 'wash away' effect of endothelium-derived relaxing factor (EDRF). To test whether EDRF could still play a role after gossypol, we used hemoglobin (n = 5) to bind EDRF. Flow-dependent constriction was still observed, although the mean diameter was decreased. We conclude that flow-dependent constriction is either mediated via the endothelial cells, but not via EDRF, or that the endothelial cells are not involved.