Predictors of difficult videolaryngoscopy with GlideScope® or C-MAC® with D-blade: secondary analysis from a large comparative videolaryngoscopy trial.

BACKGROUND: Tracheal intubation using acute-angle videolaryngoscopy achieves high success rates, but is not without difficulty. We aimed to determine predictors of 'difficult videolaryngoscopy'. METHODS: We performed a secondary analysis of a data set (n=1100) gathered from a multicentre prospective randomized controlled trial of patients for whom difficult direct laryngoscopy was anticipated and who were intubated with one of two videolaryngoscopy devices (GlideScope(®) or C-MAC(®) with D-blade). 'Difficult videolaryngoscopy' was defined as 'first intubation time >60 s' or 'first attempt intubation failure'. A multivariate logistic regression model along with stepwise model selection techniques was performed to determine independent predictors of difficult videolaryngoscopy. RESULTS: Of 1100 patients, 301 were identified as difficult videolaryngoscopies. By univariate analysis, head and neck position, provider, type of surgery, and mouth opening were associated with difficult videolaryngoscopy (P<0.05). According to the multivariate logistic regression model, characteristics associated with greater risk for difficult videolaryngoscopy were as follows: (i) head and neck position of 'supine sniffing' vs 'supine neutral' {odds ratio (OR) 1.63, 95% confidence interval (CI) [1.14, 2.31]}; (ii) undergoing otolaryngologic or cardiac surgery vs general surgery (OR 1.89, 95% CI [1.19, 3.01] and OR 6.13, 95% CI [1.85, 20.37], respectively); (iii) intubation performed by an attending anaesthestist vs a supervised resident (OR 1.83, 95% CI [1.14, 2.92]); and (iv) small mouth opening (OR 1.18, 95% CI [1.02, 1.36]). CONCLUSION: This secondary analysis of an existing data set indicates four covariates associated with difficult acute-angle videolaryngoscopy, of which patient position and provider level are modifiable.

Spinal anesthesia in an extremely low birth weight infant.

A case of spinal anesthesia in an extremely low birth weight male infant (body weight of 930 g at time of surgery) is presented. He was born prematurely at a gestational age of 27 weeks because of a placenta tumor and had to undergo inguinal herniotomy at 34 weeks postconceptional age. He had bronchopulmonary dysplasia and oxygen supply was still required because of frequent deterioration of oxygen saturation. Spinal anesthesia was performed successfully without any complications. Relevant aspects concerning the technique and management of spinal anesthesia in preterm infants are discussed.

Pharmacological preconditioning in global cerebral ischemia.

Single dose 3-nitropropionic acid (3-NPA) 24 hr before global ischemia improves neuronal survival in both, neocortex and hippocampus ('chemical preconditioning'). Neuronal survival after transient global ischemia requires new protein synthesis during recovery, especially of those with anti-apoptotic function. Bcl-2-protein is expressed in neurons that survive cerebral ischemia and may parallel the time course of tolerance after ischemic preconditioning. With this study we examined whether differences in bcl-2-protein expression compared to baseline may be involved in the induction of ischemic tolerance using 3-NPA. Male Wistar rats received either a single intraperitoneal (i.p.) dose of 3-NPA (20 mg/kg), and were observed for 3 (n = 4), 12 (n = 5) or 24 hours (n = 5) or the same amount of vehicle and were observed for 24 h (n = 8, controls). Immunohistochemistry allowed to compare the intensity of bcl-2 immunoreactivity at three subsequent time points in hippocampus, dentate gyrus and parietal neocortex with that of control animals. A single dose of 3-NPA caused a significant increase of bcl-2 protein immunoreactivity in hippocampal neurons, i.e. CA 1 (5 out of 5 animals, p = 0.003), CA 3 (5/5, p = 0.003), CA 4 (4/5, p = 0.025), and neocortex (5/5, p = 0.004), in a time dependent manner over a period of 24 hr after injection. Neuronal bcl-2 protein expression in CA 2 and dentate gyrus remained unchanged. The data suggest a possible role of bcl-2-protein in chemical induction of ischemic tolerance using a single subtoxic dose of 3-NPA. Bcl-2-protein expression may be initiated by increased levels of reactive oxygen species (ROS) after 3-NPA administration, as shown by others. Additional bcl-2 protein may then be available to (1) control postischemic ROS burst, (2) protect the mitochondrial membranes, and (3) inhibit pro-apoptotic mechanisms.

[Management of pediatric airway--anatomy, physiology and new developments in clinical practice]. / Der kindliche Atemweg--Anatomische und physiologische Besonderheiten sowie neue Erkenntnisse zum Airway-Management in der klinischen Praxis.

Due to the special features of paediatric anatomy and physiology, the expected and unexpected difficult paediatric airway is one of the major challenges to every anaesthesiologist, paediatrician and emergency physician. During the last years, some new devices have been made available to improve airway management in children and infants, and several studies have advanced our understanding of the risks and benefits of our clinical practice. Certain risk factors for airway related problems during anaesthesia in children having a "cold" have been identified, and there are new aspects of the controversy concerning the use of cuffed endotracheal tube (ETT) in children. New video assisted systems have been introduced for the management of the difficult airway in paediatric patients, and new applications for well-known devices have been suggested, e.g. the laryngeal mask airway (LMA) serving as guidance for fibreoptic intubation. Recent studies have also demonstrated specific problems with the LMA in infants, as well as possible advantages of a new prototype LMA for children, similar to the ProSeal. Furthermore, the following review presents data about the use of the Cuffed Oropharyngeal Airway (COPA) and the Laryngeal Tube (LT) in paediatric patients.

[Paracetamol in childhood. Current state of knowledge and indications for a rational approach to postoperative analgesia]. / Paracetamol im Kindesalter Aktueller Wissensstand und Hinweise für einen rationalen Einsatz zur postoperativen Analgesie.

The administration of paracetamol (in the US known as acetaminophen) to children and infants for postoperative pain after minor surgery is a well established and safe treatment option, if appropriately used. However, if paracetamol is dosed according to traditional recommendations (about 20 mg/kg body weight) frequently a sufficient analgetic effect cannot be achieved immediately after painful interventions. Recently, a higher initial dose (40 mg/kg body weight) was suggested for effective postoperative pain control, which seems especially important for children after ambulatory anesthesia, but may also be associated with certain risks to the patient. Current recommendations also involve appropriate timing and route of administration of paracetamol to be most effective under different clinical circumstances. In contrast, the risk for liver toxicity appears to be very low, if the daily paracetamol dose does not exceed 90 mg/kg body weight in otherwise healthy children, and if specific risk factors of the individual patient are always considered. This review discusses the recent publications on pharmacokinetics and -dynamics, the clinical use and dosing, as well as the risks and benefits of paracetamol for the treatment of postoperative pain in children and infants. Based on this information, specific dosing regimes for the postoperative period are suggested for neonates and infants, as well as for children in different age groups.

Failure to sustain recovery of Na,K-ATPase function is a possible mechanism for striatal neurodegeneration in hypoxic-ischemic newborn piglets.

Hypoxia-ischemia (HI) in the newborn can lead to a variety of sensorimotor abnormalities, including movement and posture disorders. Striatal neurons undergo necrosis after HI in piglets, but mechanisms for this neuronal death are not understood. We tested the hypothesis that Na,K-ATPase is defective in striatum early after HI. Piglets (1 week old) were subjected to 30 min hypoxia (arterial oxygen saturation 30%) and then 7 min of airway occlusion (oxygen saturation 5%), producing asphyxic cardiac arrest. Animals were resuscitated and recovered for 3, 6, 12, and 24 h, respectively. Neuronal necrosis in the striatum is progressive [14]. Na,K-ATPase activity (percent of control) was 60, 98, 51, and 54% at 3, 6, 12, and 24 h after HI, respectively. Intrastriatal differences in enzyme activity were detected histochemically, with the putamen showing greater loss of Na,K-ATPase activity than caudate after 12 h recovery. Immunoblotting showed that the levels of the alpha(3) isoform (localized exclusively to neurons) were 85, 115, 101, and 79% of sham control at 3, 6, 12, and 24 h, respectively. Levels of beta(1), the predominant beta isoform, were similar to alpha(3), while levels of the alpha(1) subunit, the catalytic isoform found in neurons and glia, were 182, 179, 226, and 153% at the same recovery times. We conclude that early inactivation of Na,K-ATPase function participates in the pathogenesis of striatal neuron necrosis, but that loss of enzyme function early after HI is not caused by depletion of composite alpha/beta subunits.

Tolerance-Inducing dose of 3-nitropropionic acid modulates bcl-2 and bax balance in the rat brain: a potential mechanism of chemical preconditioning.

Many studies have reported ischemia protection using various preconditioning techniques, including single dose 3-nitropropionic acid (3-NPA), a mitochondrial toxin. However, the cellular signal transduction cascades resulting in ischemic tolerance and the mechanisms involved in neuronal survival in the tolerant state still remain unclear. The current study investigated the mRNA and protein expression of the antiapoptotic bcl-2 and the proapoptotic bax. two antagonistic members of the bcl-2 gene family, in response to a single dose of 3-NPA, to global cerebral ischemia-reperfusion. and to the combination of both 3-NPA-pretreatment and subsequent global cerebral ischemia-reperfusion. Brain homogenates of adult Wistar rats (n = 25) were analyzed for bcl-2 and bax mRNA expression using a new highly sensitive and quantitative polymerase chain reaction (PCR) technique that allows real-time fluorescence measurements of the PCR product (LightCycler; Roche Diagnostics, Mannheim, Germany). Animals for mRNA analysis received 3-NPA (20 mg/kg, intraperitoneal; "chemical preconditioning") or vehicle (normal saline), and were either observed for 24 plus 3 hours or were subjected to 15 minutes of global cerebral ischemia 24 hours after the pretreatment and observed for 3 hours of reperfusion. Immunohistochemistry was applied to serial brain sections of additional rats (n = 68) to determine amount and localization of the respective Bcl-2 and Bax protein expression in various brain areas. One set of animals was injected with 3-NPA and observed for 3, 12, 24, and 96 hours; a second set was exposed to 15 minutes global cerebral ischemia, 3, 12, and 24 hours reperfusion; and a third set was pretreated with 3-NPA or saline 24 hours before the ischemic brain insult and observed for 96 hours of reperfusion. The authors found single dose 3-NPA treatment to be associated with an elevated bcl-2:bax ratio (increased bcl-2 expression, decreased bax expression), both on the transcriptional (mRNA) and the translational (protein) level. The differential influence of 3-NPA was maintained during early recovery from global cerebral ischemia (3 hours), when 3-NPA pretreated animals showed higher bcl-2 and lower bax mRNA levels compared with rats with saline treatment. Respective changes in protein expression were localized predominately in neurons vulnerable to ischemic damage. Compared with baseline, Bcl-2 protein was significantly higher in surviving neurons at 96 hours after the insult, whereas Bax protein remained unchanged. However, at this late time of postischemic recovery (96 hours), the protein expression pattern of surviving neurons was not different between animals with and without 3-NPA pretreatment. To the authors' knowledge, the current study is the first report on the differential expression of pro- and antiapoptotic genes after a single, nonlethal dose of 3-NPA. The current results suggest alterations in the balance between pro- and antiapoptotic proteins as a potential explanation for the reported protection provided by chemical preconditioning using 3-NPA in rats.

Neuronal death in newborn striatum after hypoxia-ischemia is necrosis and evolves with oxidative stress.

The mechanisms for neurodegeneration after hypoxia-ischemia (HI) in newborns are not understood. We tested the hypothesis that striatal neuron death is necrosis and evolves with oxidative stress and selective organelle damage. Piglets ( approximately 1 week old) were used in a model of hypoxia-asphyxia and survived for 3, 6, 12, or 24 h. Neuronal death was progressive over 3-24 h recovery, with approximately 80% of putaminal neurons dead at 24 h. Striatal DNA was digested randomly at 6-12 h. Ultrastructurally, dying neurons were necrotic. Damage to the Golgi apparatus and rough endoplasmic reticulum occurred at 3-12 h, while most mitochondria appeared intact until 12 h. Mitochondria showed early suppression of activity, then a transient burst of activity at 6 h, followed by mitochondrial failure (determined by cytochrome c oxidase assay). Cytochrome c was depleted at 6 h after HI and thereafter. Damage to lysosomes occurred within 3-6 h. By 3 h recovery, glutathione levels were reduced, and peroxynitrite-mediated oxidative damage to membrane proteins, determined by immunoblots for nitrotyrosine, occurred at 3-12 h. The Golgi apparatus and cytoskeleton were early targets for extensive tyrosine nitration. Striatal neurons also sustained hydroxyl radical damage to DNA and RNA within 6 h after HI. We conclude that early glutathione depletion and oxidative stress between 3 and 6 h reperfusion promote damage to membrane and cytoskeletal proteins, DNA and RNA, as well as damage to most organelles, thereby causing neuronal necrosis in the striatum of newborns after HI.

Successful treatment of a patient with ARDS after pneumonectomy using high-frequency oscillatory ventilation.

High frequency oscillatory ventilation (HFOV) was used in a patient who developed the acute respiratory distress syndrome 5 days following a right pneumonectomy for bronchogenic carcinoma. When conventional pressure-controlled ventilation failed to maintain adequate oxygenation, HFOV dramatically improved oxygenation within the first few hours of therapy. Pulmonary function and gas exchange recovered during a 10-day period of HFOV. No negative side effects were observed. Early use of HFOV may be a beneficial ventilation strategy for adults with acute pulmonary failure, even in the postoperative period after lung resection.

Effect of arrest time and cerebral perfusion pressure during cardiopulmonary resuscitation on cerebral blood flow, metabolism, adenosine triphosphate recovery, and pH in dogs.

OBJECTIVES: To test the hypothesis that greater cerebral perfusion pressure (CPP) is required to restore cerebral blood flow (CBF), oxygen metabolism, adenosine triphosphate (ATP), and intracellular pH (pHi) levels after variable periods of no-flow than to maintain them when cardiopulmonary resuscitation (CPR) is started immediately. DESIGN: Prospective, randomized, comparison of three arrest times and two perfusion pressures during CPR in 24 anesthetized dogs. SETTING: University cerebral resuscitation laboratory. INTERVENTIONS: We used radiolabeled microspheres to determine CBF and magnetic resonance spectroscopy to derive ATP and pHi levels before and during CPR. Ventricular fibrillation was induced, epinephrine administered, and thoracic vest CPR adjusted to provide a CPP of 25 or 35 mm Hg after arrest times of O, 6, or 12 mins. MEASUREMENTS AND MAIN RESULTS: When CPR was started immediately after arrest with a CPP of 25 mm Hg, CBF and ATP were 57 +/- 10% and 64 +/- 14% of prearrest (at 10 mins of CPR). In contrast, CBF and ATP were minimally restored with a CPP at 25 mm Hg after a 6-min arrest time (23 +/- 5%, 16 +/- 5%, respectively). With a CPP of 35 mm Hg, extending the no-flow arrest time from 6 to 12 mins reduced reflow from 71 +/- 11% to 37 +/- 7% of pre-arrest and reduced ATP recovery from 60 +/- 11% to 2 +/- 1% of pre-arrest. After 6- or 12-min arrest times, brainstem blood flow was restored more than supratentorial blood flow, but cerebral pHi was never restored. CONCLUSIONS: A CPP of 25 mm Hg maintains supratentorial blood flow and ATP at 60% to 70% when CPR starts immediately on arrest, but not after a 6-min delay. A higher CPP of 35 mm Hg is required to restore CBF and ATP when CPR is delayed for 6 mins. After a 12-min delay, even the CPP of 35 mm Hg is unable to restore CBF and ATP. Therefore, increasing the arrest time at these perfusion pressures increases the resistance to reflow sufficient to impair restoration of cerebral ATP.

Effects of propofol (intravenous propofol emulsion) on cell membranes measured by electrofusion and electroporation.

The influence of propofol (CAS 2078-54-8 (intravenous propofol emulsion) on cell membrane properties was investigated in vitro with techniques of cell electrofusion and cell electroporation. Human lymphoma cells and plant protoplasts were chosen as a model system. Propofol (intravenous propofol emulsion) decreased the electrofusion yield of the cells and their membrane permeability. A 50% decrease in relative electrofusion was observed in human lymphoma cells in the presence of about 0.05 mmol/l propofol (intravenous propofol emulsion) and in plant protoplasts in the presence of about 0.1 mmol/l. The fusion of human lymphoma cells was inhibited to 100% at concentrations higher than 0.2 mmol/l propofol and 0.4 mmol/l intravenous propofol emulsion. The membrane permeability of human lymphoma cells decreased by the factor of two with increasing propofol concentrations up to about 0.1 mmol/l. The effects of electroporation were highly reversible. Propofol (intravenous propofol emulsion) was more effective than tetracaine. These sensitive techniques are suitable for the investigation of interactions between anesthetic drugs and the cell membrane.

Effects of normobaric oxygen on ciliary beat frequency of human respiratory epithelium.

Respiratory infection is a major cause of morbidity after general anaesthesia. Impairment of respiratory ciliary beat frequency (CBF) by different stress factors causes a decrease in mucus transport rate (MTR). We have tested the effect of different concentrations of oxygen on CBF of human respiratory epithelium in a prospective, randomized, in vitro study. Samples of superficial mucosa of the inferior nasal turbinates of 20 non-smoking healthy volunteers were harvested and exposed to three different oxygen environments (group I = 21% oxygen, group II = 60% oxygen and group III = 95% oxygen) for 2 h. In 50% of the samples, exposure time was prolonged. At 30, 60, 90, 120 and 240 min, light microscopic images of cilia activity were videotaped and CBF was later assessed in slow motion. Compared with baseline, group I showed no difference in CBF throughout the study. CBF was increased in group II from mean 9.7 (SD 0.4) to 11.2 (0.4) Hz (16%, P < 0.001) and in group III from 9.5 (0.6) to 12.1 (0.5) Hz (28%, P < 0.001) at 120 min. After 240 min of exposure to 95% oxygen, the CBF trend in group III was reduced to 11.8 (0.6) Hz but still remained above baseline. We conclude that oxygen appeared to have a dose- and time-dependent accelerating effect on CBF. Prolonged exposure to high oxygen concentrations reversed this trend. Direct oxygen toxicity ("oxygen stress") is a possible explanation for this effect. These changes may result in impaired MTR.

[Neurogenic pulmonary edema. Pathogenesis, clinical picture and therapy]. / Das neurogene Lungenödem. Pathogenese, Kilinik und Therapie.

UNLABELLED: Neurogenic pulmonary edema (NPE) is a rare but always life-threatening complication in patients with central nervous system lesions. NPE is evident if patients shortly after cerebral lesions suddenly develop pulmonary edema and other causes of the symptoms, such as aspiration of gastric content, congestive heart failure and direct toxic exposure, are ruled out. METHODS: The current body of literature, partially obtained by computer-guided search (Winspirs) regarding epidemiology, pathophysiology and therapy of NPE was reviewed. Additionally, the case of a patient who developed a sudden pulmonary edema after an episode of tonic-clonic seizures is analyzed. We first provide information about history, definition, incidence and mortality of NPE. Second, a case report of a postictal NPE is presented to illustrate the clinical picture of NPE, and the applied therapeutic strategies are discussed. Third, recent pathophysiologic concepts about symptoms and possible therapeutic principles are reviewed. Fourth, a rational therapeutic plan for the prehospital emergency therapy of NPE is outlined. RESULTS: The different etiologies all have one characteristic feature: an acute emergency which causes increased intracerebral pressure (ICP). NPE is known in patients after cerebral trauma, intracranial hemorrhage, stroke, intracranial tumor or seizures. The incidence is estimated at around 1% after cerebral trauma, at 71% after cerebral hemorrhage and at 2% after seizures. Mortality is appraised to lie between 60 and 100%, independent of etiology. There is a definite pathophysiologic sequence leading to NPE: a central nervous system lesion causes a sudden increase in ICP which triggers an upregulation of sympathetic signal transduction to assure brain perfusion. Increased tonus of venous and arterial vessels and of myocardial function are the immediate consequences. However, if systemic vascular resistance (SVR) increases excessively, left ventricular failure and finally pulmonary edema (NPE) may result. Additionally, the protein-rich edema fluid points to an increased endothelial permeability within the pulmonary circuit. This is thought to be caused by the acute pressure increase and by neurohumoral mechanisms, possibly similar to those described for the systemic inflammatory response syndrome (SIRS). The most important central nervous system structures involved in NPE are the medulla oblongata and the hypothalamus. CONCLUSION: NPE is always a life-threatening symptom after increased ICP, where immediate therapeutic interventions are imperative. A rational therapeutic approach needs to be focused on decreasing ICP as primary goal. Additionally, attempts should be made to optimize body oxygenation, decrease pre- and afterload and increase myocardial contractility. Postictal patients suspicious for incipient ventilation problems must be admitted to hospital for further evaluation.