Airway management in craniofacial trauma patients is a challenge for an anesthetist. Treating these patients requires a close interdisciplinary communication and cooperation. Maintaining the airway and oxygenation of the patient is the initial challenge in craniofacial trauma patients. The management of the difficult airway is facilitated and patient's safety improved by following one of several published difficult airway algorithms. We describe the St. Gallen difficult airway algorithm for the management of difficult airway in general and the airway in facial trauma patients in particular. Whenever possible, the airway should be secured in a conscious and spontaneously breathing patient. It is important to be familiar with different techniques and to change the approach after two unsuccessful attempts with one technique. Once the airway is established, all available preventive measures should be used to avoid losing the airway. A tracheotomy has its place in a significant number of patients in whom an immediate postoperative or a delayed extubation appears unfeasible.
The present study compares the changes in ventilation in response to sustained hypobaric hypoxia and acute normobaric hypoxia between subjects susceptible to high altitude pulmonary edema (HAPE-S) and control subjects (C-S). Seven HAPE-S and five C-S were exposed to simulated high altitude of 4000 m for 23 h in a hypobaric chamber. Resting minute ventilation (V(E)), tidal volume (V(T)), and respiratory frequency (f(R)), as well as the end-tidal partial pressures of oxygen (P(ET(O2))) and carbon dioxide (P(ET(CO2))) were measured in all subjects sitting in a standardized position. Six measurement periods were recorded: ZH1 at 450 m at Zurich level, HA1 on attaining 3600 m altitude, HA2 after 20 min at 4000 m, HA3 after 21 h and HA4 after 23 h at 4000 m altitude, and ZH2 immediately after recompression to Zurich level. At ZH1 and HA3, the measurements were first done in lying, then in sitting, and afterwards in standing. Peripheral arterial oxygen saturation (Sa(O2)) was continuously recorded. All respiratory parameters were also measured during exercise lasting 30 min, the work load being 50% of maximal oxygen consumption (V(O2max)) at Zurich level and 26% of the Zurich V(O2max) at 4000 m. V(E), P(ET(O2)) and P(ET(CO2)) did not significantly differ between HAPE-S and C-S at rest and during exercise periods at Zurich level and at high altitude. However, Sa(O2) was significantly lower in HAPE-S than in C-S at rest and during exercise at 4000 m. Breathing through the mouthpiece during ventilation measurements increased significantly the Sa(O2) in HAPE-S in posture tests at HA3. This effect was most pronounced in the supine posture, in which HAPE-S had the lowest Sa(O2) values. These data provide evidence that (1) gas exchange might be impaired on the level of ventilation-perfusion mismatch or due to diffusion limitation in HAPE-S during the first 23 h of exposure to a simulated altitude of 4000 m, and (2) contrary to C-S, the Sa(O2) in HAPE-S is significantly affected by body position and by mouthpiece breathing.
Many anesthesia textbooks advise anesthesiologists to demonstrate that ventilation with a facemask is possible before giving muscle relaxants. This recommendation is not evidence-based. If a functional airway obstruction is responsible for difficult mask ventilation and with high induction doses it will rarely be possible for the patient to recover spontaneous ventilation before hypoxia develops. Muscle relaxants improve facemask ventilation and facilitate tracheal intubation. With early administration of muscle relaxants good intubation conditions are achieved earlier. The recommendation does not include a definition of successful mask ventilation and makes the decision in critical situations ambiguous. This is probably one of the reasons why most anesthesiologists administer muscle relaxants even though mask ventilation is difficult or impossible. Therefore the authors recommend giving muscle relaxants after loss of consciousness and thereafter starting gentle bag mask ventilation. To prevent a cannot ventilate cannot intubate situation patient airways have to be carefully evaluated preoperatively. If difficult ventilation or intubation is expected an alternative procedure should be chosen.
Objective To examine the effects of short-term cyclic stretch on apoptosis in alveolar type II cells (A549). To study in vitro the direct influence of alveolar type II cells on mechanical stretch. Methods A549 were treated with different doses of lipopolysaccharide (LPS), 0 ng/ml, 1 ng/ml, 10 ng/ml, 100 ng/ml, 1000 ng/ml, and then A549 were lengthened 5%, 15%, 30% using a FLEXCELL tension unit 4000, a vacuum-driven device that applies strain to cells, which were cultured in six-well plates coated with collagen-I, and 12 cycles/min for 4 hours. Apoptosis was measured using the flow cytometry method that measures annexin V and propidium iodide (PI) staining. The morphological changes of apoptotic cells were observed by transmission electron microscope. Results Apoptosis could be induced in alveolar type II cells (A549) by mechanical stretch. The percentage of annexin V + PI cells increased after being treated with cyclic stretch for 4 hours by 5%, 15%, 30% in all groups. The morphological features of apoptotic cells demonstrated by transmission electron microscope were as follows: shrinkage of the cell, chromatin condensation and aggregation under the nuclear membrane as a crescent or lump, membrane-encapsulated nuclear fragment or cell organ formed by invagination of the cell membrane, and apoptotic body formation followed by vacuolization. Conclusion Apoptosis induced by mechanical stretch and LPS is dose dependent. Mechanical stretch aggravates apoptosis especially in cells treated with LPS. Annexin V and PI double staining is a specific, sensitive, and quantitative method for analyzing apoptotic cells. It is also helpful to clarify the protective mechanism of low-volume ventilation in ARDS. Acknowledgement The study was funded by the 'One Hundred People' project of Shanghai Sanitary Bureau (03-77-20). Introduction Although extrapulmonary ALI/ARDS is a common clinical entity, most animal models used to study this disease are induced by direct lung injuries. Our intention was therefore to investigate whether a condition resembling ALI/ARDS develops during the course of a fecal peritonitis in pigs; in that case experimental peritonitis would also prove as a clinically relevant ARDS model. Methods In 10 anesthetized, mechanically ventilated, and instrumented pigs fecal peritonitis was induced by inoculating autologue feces pellets suspended in saline. Mechanical ventilation was set with VT = 8 ml/kg, FiO 2 to reach a SaO 2 target of >90%, PEEP = 10 cmH 2 O if PaO 2 /FiO 2 > 300 and 12 cmH 2 O if PaO 2 /FiO 2 < 300, and respiratory rate to obtain a PaCO 2 of 35-45 mmHg. Before as well as 12 and 24 hours after peritonitis induction we measured the PaO 2 /FiO 2 ratio, the total compliance of the respiratory system (C), calculated as VT/(P plateau -PEEP) and inspiratory airway resistance (R i ) calculated as (P max -P plateau ) / mean inspiratory flow. Data are mean [range]. Results For data see Table 1. During the course of the 24-hour study period, six of 10 animals developed gas exchange deteriorations consistent w...
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