Prehospital management of patients with suspected acute coronary syndrome : Real world experience reflecting current guidelines.

BACKGROUND: In case of suspected acute coronary syndrome (ACS), international guidelines recommend to obtain a 12-lead ECG as soon as possible after first medical contact, to administrate platelet aggregation inhibitors and antithrombins, and to transfer the patient as quickly as possible to an emergency department. METHODS: A German emergency care service database was retrospectively analysed from 2014 to 2016. Data were tested for normal distribution and the Mann-Whitney test was used for statistical analysis. Results are presented as medians (IQR). RESULTS: A total of 1424 patients with suspected ACS were included in the present analysis. A 12-lead ECG was documented in 96% of patients (n = 1369). The prehospital incidence of ST-segment elevation myocardial infarction (STEMI) was 18% (n = 250). In 981 patients (69%), acetylsalicylic acid (ASA), unfractionated heparin (UFH), or ASA and UFH was given. Time in prehospital care differed significantly between non-STEMI (NSTEMI) ACS (37 [IQR 30, 44] min) and STEMI patients (33 [IQR 26, 40] min, n = 1395, p < 0.0001). Most of NSTEMI ACS and STEMI patients were brought to the emergency care unit, while 30% of STEMI patients were directly handed over to a cardiac catheterization laboratory. CONCLUSIONS: Prehospital ECG helps to identify patients with STEMI, which occurs in 18% of suspected ACS. Patients without ST-elevations suffered from longer prehospital care times. Thus, it is tempting to speculate that ST-elevations in patients prompt prehospital medical teams to act more efficiently while the absence of ST-elevations even in patients with suspected ACS might cause unintended delays. Moreover, this analysis suggests the need for further efforts to make the cardiac catheterization laboratory the standard hand-over location for all STEMI patients.

[Acute Respiratory Failure after Silicone Injection]. / Akutes respiratorisches Versagen durch Silikon-Injektion.

A 35-year-old male patient presented to the emergency department with complains of fever, dyspnea and petechiae. The chest X-ray revealed signs of bipulmonary infiltration. 5 days ago, an illicit silicone injection was performed into the penis for cosmetic reasons. Due to progressive respiratory failure the patient required mechanical ventilation. Bronchoalveolar lavage revealed diffuse alveolar hemorrhage. Silicone pneumonitis with a severe acute respiratory failure based on silicone embolization syndrome was diagnosed. Prone positioning, lung-protective ventilation and corticosteroid therapy were initiated. The patient was discharged from ICU after 19 days. In an outpatient follow up, lung function was fully recovered. CONCLUSION: Silicone pneumonitis should be considered in case of fever, respiratory distress and alveolar hemorrhage linked to cosmetic procedures. High dose corticosteroid therapy and lung-protective ventilation strategies may help for complete recovery of lung function.

[Update in neuroanesthesiology - key publications]. / Neuroanästhesiologisches Update ­ Schlüsselpublikationen.

One of the aims of the Scientific Working Group Neuroanesthesia (WAKNA) of the German Society of Anesthesiology and Intensive Care Medicine is to disseminate new findings in the field of neuroscience and neuroanesthesia and to propagate novel therapeutic and diagnostic options into clinical practice. Once a year, the WAKNA displays and discusses recent noteworthy publications from the past 12 months at the German Anesthesia Meeting. In 2016, a new pharmacologic strategy with dexmedetomidine to prevent postoperative pain after craniotomy, the impact of the widely used anesthetic drug propofol on GABA receptor surface expression, a study highlighting the ultrasound-guided detection of increased intracranial pressure, and an article showing the interactions of neuromuscular blocking drugs on the BIS neuromonitoring were presented.

Intrajugular balloon catheter reduces air embolism in vitro and in vivo.

BACKGROUND: Neurosurgical procedures requiring a sitting position may put the patient at risk of a potentially life-threatening air embolism. Transient manual jugular venous compression limits further air entry in this situation. This study presents an alternative technique aimed at reducing the risk of air embolism. METHODS: In an in vitro model, an intrajugular balloon catheter was inserted to demonstrate that this device prevents air embolism. In an in vivo study, this device was bilaterally placed into jugular vessels in pigs. Using an ultrasound technique, blood flow was monitored and jugular venous pressure was recorded before and during cuff inflation. Air was applied proximally to the inflated cuffs to test the hypothesis that this novel device blocks air passage. RESULTS: In vitro, the intrajugular balloon catheter reliably prevented further air entry (n=10). Additionally, accumulated air could be aspirated from an orifice of the catheter (n=10). In vivo, inflation of the catheter balloon completely obstructed venous blood flow (n=8). Bilateral inflation of the cuff significantly increased the proximal jugular venous pressure from 9.8 (2.4) mm Hg to 14.5 (2.5) mm Hg (n=8, P<0.05). Under conditions mimicking an air embolism, air passage across the inflated cuffs was prevented and 78 (20%) (n=6) of the air dose could be aspirated by the proximal orifice of the catheter. CONCLUSIONS: These findings may serve as a starting point for the development of intrajugular balloon catheters designed to reduce the risk of air embolism in patients undergoing neurosurgery in a sitting position.

Propofol modulates phasic and tonic GABAergic currents in spinal ventral horn interneurones.

BACKGROUND: Surgical interventions like skin incisions trigger withdrawal reflexes which require motor neurones and local circuit interneurones in the spinal ventral horn. This region plays a key role in mediating immobilizing properties of the GABAergic anaesthetic propofol. However, it is unclear how propofol modulates GABA(A) receptors in the spinal ventral horn and whether tonic or phasic inhibition is involved. METHODS: Organotypic spinal cord tissue slices were prepared from mice. Whole-cell recordings were performed for quantifying effects of propofol on GABA(A) receptor-mediated phasic transmission and tonic conductance. RESULTS: Propofol increased GABAergic phasic transmission by a prolongation of the decay time constant in a concentration-dependent manner. The amount of the charge transferred per inhibitory post-synaptic current, described by the area under the curve, was significantly augmented by 1 µM propofol (P<0.01). A GABA(A) receptor-mediated tonic current was not induced by 1 µM propofol but at a concentration of 5 µM (P<0.05). CONCLUSIONS: Propofol depresses ventral horn interneurones predominantly by phasic rather than by tonic GABA(A) receptor-mediated inhibition. However, the present results suggest that the involvement of a tonic inhibition might contribute to the efficacy of propofol to depress nociceptive reflexes at high concentrations of the anaesthetic.

4-bromopropofol decreases action potential generation in spinal neurons by inducing a glycine receptor-mediated tonic conductance.

BACKGROUND AND PURPOSE: Impaired function of spinal strychnine-sensitive glycine receptors gives rise to chronic pain states and movement disorders. Therefore, increased activity of glycine receptors should help to treat such disorders. Although compounds targeting glycine receptors with a high selectivity are lacking, halogenated analogues of propofol have recently been considered as potential candidates. Therefore we asked whether 4-bromopropofol attenuated the excitability of spinal neurons by promoting glycine receptor-dependent inhibition. EXPERIMENTAL APPROACH: The actions of sub-anaesthetic concentrations of propofol and 4-bromopropofol were investigated in spinal tissue cultures prepared from mice. Drug-induced alterations in action potential firing were monitored by extracellular multi-unit recordings. The effects on GABAA and glycine receptor-mediated inhibition were quantified by whole-cell voltage-clamp recordings. KEY RESULTS: Low concentrations of 4-bromopropofol (50 nM) reduced action potential activity of ventral horn neurons by about 30%, compared with sham-treated slices. This effect was completely abolished by strychnine (1 µM). In voltage-clamped neurons, 4-bromopropofol activated glycine receptors, generating a tonic current of 65 ± 10 pA, while GABAA - and glycine receptor-mediated synaptic transmission remained unaffected. CONCLUSIONS AND IMPLICATIONS: The highest glycine levels in the CNS are found in the ventral horn of the spinal cord, a region mediating pain-induced motor reflexes and participating in the control of muscle tone. 4-Bromopropofol may serve as a starting point for the development of non-sedative, non-addictive, muscle relaxants and analgesics to be used to treat low back pain.

[Precipitation of piritramide and cefazolin. Study of the dependence on concentration and pH]. / Präzipitation von Piritramid und Cefazolin. Untersuchungen zur Abhängigkeit von Konzentration und pH.

BACKGROUND: Drug incompatibility might lead to precipitation with subsequent serious complications, such as transient pulmonary embolism. Recently, incompatibility of the opioid piritramide with cephalosporin antibiotics was described. As both drugs are frequently administered in a perioperative setting, the present study addressed the question whether the precipitation effect depends on the piritramide concentration or on the pH of the solution. Moreover, it was tested whether the precipitate reversibly dissolves in a physiological saline solution. METHODS: Piritramide was diluted to the final test concentrations in 0.9 % sodium chloride solution. Precipitation tests were performed by combining 1 ml of the respective piritramide dilution with 1 ml of cefazolin (20 mg/ml) in a syringe. Precipitation was detected by visual inspection as an opaque whitish appearance of the mixture. Each concentration was tested 5 times. The pH values of the tested piritramide concentrations were determined using a 3-point calibrated pH meter. The precipitate formed in 1 ml of cefazolin (20 mg/ml) and 1 ml of piritramide (5 mg/ml) was diluted in 3 ml physiological saline. RESULTS: The piritramide concentrations 5 mg/ml, 3.75 mg/ml and 3 mg/ml precipitated in the presence of cefazolin (20 mg/ml), while the concentrations 1.875 mg/ml, 1 mg/ml and 0.5 mg/ml did not produce a precipitate. To exclude the possibility that changes in pH of the tested dilutions might be responsible for these findings, the pH values of the piritramide dilutions were measured. The mean pH values of the concentrations 5 mg/ml, 3.75 mg/ml, 3 mg/ml, 1.875 mg/ml and 1 mg/ml did not differ significantly (pH 3.89 ± 0.004, n = 26, tested by ANOVA). However, the mean pH of 0.5 mg/ml was significantly different from the other tested dilutions (pH 3.98 ± 0.02, n = 6; p < 0.01 by ANOVA). After diluting the precipitate of piritramide and cefazolin in physiological saline the whitish precipitate completely dissolved and the resulting solution became clear (n = 5). CONCLUSION: The results imply a concentration dependence of the precipitation with cefazolin, while a correlation with pH changes could not be detected. In cases of co-administration of cephalosporins and piritramide, a piritramide concentration of 1 mg/ml seems to be safe and does not form a precipitate. As the precipitate could be reversed by diluting in saline solution it is most likely that a proton switch between the carboxylic acid moiety of cefazolin and the amino group of piritramide causes the precipitation.

ALX 1393 inhibits spontaneous network activity by inducing glycinergic tonic currents in the spinal ventral horn.

BACKGROUND: Strychnine-sensitive glycine receptors are activated by glycine and facilitate chloride influx into neurons. Glycinergic transmission might be either mediated by synaptic or extrasynaptic glycine receptors. While phasic neurotransmission is provided by a synaptic pathway, activation of extrasynaptic glycine receptors induces tonic inhibition. The glycine transporter 2 (GlyT2) regulates the uptake of glycine into presynaptic boutons. It is not determined yet, whether inhibition of GlyT2 by ALX 1393 can produce inhibition of spinal motoric networks and, whether phasic or tonic glycinergic inhibition is mostly enhanced. METHODS: We investigated the effect of ALX 1393 on spontaneous action potential firing activity by extracellular recordings in the ventral horn area of organotypic spinal cultures. Additionally, using the whole-cell patch-clamp technique, we defined the influence of GlyT2 inhibition on tonic and phasic glycinergic transmission in commissural interneurons of the ventral horn. RESULTS: GlyT2 inhibition by ALX 1393 potently reduced neuronal action potential activity in a concentration-dependent manner (n=211). The half maximal effect of ALX 1393 was observed at 100 ± 31 nM. Moreover, 88.3 ± 2.6% of the action potential activity was suppressed at 1 µM. Whole-cell patch-clamp recordings unveiled that ALX 1393 (200 nM) induced a tonic current (-45.7 ± 11.6 pA, n=5) that was significantly reversed by application of the competitive glycine receptor antagonist strychnine. Contrastingly, phasic glycinergic transmission was not augmented by GlyT2 inhibition (charge transferred per time period for control conditions: 1.1 ± 0.1 pC, n=7, for ALX 1393: 0.9 ± 0.2 pC, n=7, p>0.05). CONCLUSION: GlyT2 inhibition induced glycinergic tonic currents, which might be the underlying mechanism for the observed suppression of spontaneous action potential activity by ALX 1393 in the spinal ventral horn. Silencing neuronal action potential activity by blocking GlyT2 might be a novel principle to inhibit locomotor circuits in the ventral horn area and to induce muscle relaxation.

[General practitioner's medical records for preoperative anesthetic visit]. / Risiken minimieren, Patientenbelastung reduzieren, Kosten sparen. Narkosevorbereitung beim Hausarzt: Worauf kommt es an?

General practitioners' medical records could deliver important information for pre-anesthesia evaluation. However, sometimes after hospital admission tests--already done by the general practitioner--have to be repeated for preoperative assessment due to incomplete information or more technical issues.These time-spending double examinations cause additional costs for the health system and discomfort for the patient. Here, we focus on important medical records patient could easily get from his general practitioner for the preoperative visit.

[What do we know about anesthetic mechanisms?: hypnosis, unresponsiveness to surgical incision and amnesia]. / Was wissen wir über Narkosemechanismen? : Bewusstlosigkeit, Bewegungslosigkeit und Amnesie.

Despite the increase of molecular knowledge in anesthesia research over the past decades there is still ongoing discussion about the mechanisms of anesthesia. This article focuses on presenting anesthetic sensitive ligand and voltage gated ion channels. The impact on anesthetic modulated ion channels is summarized for clinically commonly used anesthetics isoflurane, propofol and ketamine. Furthermore, the anesthetic features hypnosis, unresponsiveness to surgical incision and amnesia and their putative relevant anatomical sites in the central nervous system are briefly introduced.