Video vs. direct laryngoscopy for adult surgical and intensive care unit patients requiring tracheal intubation: a systematic review and meta-analysis of randomized controlled trials.

OBJECTIVE: This systematic review and meta-analysis aimed to determine whether a specific videolaryngoscopy technique is superior to standard direct laryngoscopy using a Macintosh blade to reduce the risk of difficult intubation in surgical and intensive care unit patients. MATERIALS AND METHODS: We identified all randomized controlled trials comparing videolaryngoscopes (VLSs) to direct laryngoscopy in the Cochrane Central Register of Controlled Trials, MEDLINE, and EMBASE (from inception to April 2020). The primary outcome was difficult intubation in adult surgical and intensive care unit patients. Secondary outcomes were successful intubation at the first attempt, airway trauma, sore throat, hoarseness, hypoxia, and mortality. RESULTS: We included 97 randomized controlled trials to evaluate 12775 patients. A high risk of bias was found in at least 50% of the included studies for each outcome. VLSs reduced the risk of difficult intubation compared to direct Macintosh laryngoscopy (RR 0.48, 95% CI from 0.35 to 0.65). VLSs increased the rate of successful intubation at the first attempt when compared to direct Macintosh laryngoscopy (RR 1.03, 95% CI from 1.00 to 1.07). Lower risks of airway trauma were found with VLSs (RR 0.69, 95% CI from 0.55 to 0.86). A decreased risk of hoarseness was associated with the use of VLSs (RR 0.67, 95% CI from 0.54 to 0.83). In addition, VLSs did not significantly reduce the risk of hypoxia compared with direct laryngoscopy (RR 0.83, 95% CI from 0.60 to 1.16). CONCLUSIONS: In this systematic review and meta-analysis, we found that the use of VLSs reduced the risk of difficult intubation and slightly increased the ratio of successful intubation at the first attempt among adult patients.

Spontaneous breathing during ventilatory support improves ventilation-perfusion distributions in patients with acute respiratory distress syndrome.

Ventilation-perfusion (V A/Q) distributions were evaluated in 24 patients with acute respiratory distress syndrome (ARDS), during airway pressure release ventilation (APRV) with and without spontaneous breathing, or during pressure support ventilation (PSV). Whereas PSV provides mechanical assistance of each inspiration, APRV allows unrestricted spontaneous breathing throughout the mechanical ventilation. Patients were randomly assigned to receive APRV and PSV with equal airway pressure limits (Paw) (n = 12) or minute ventilation (V E) (n = 12). In both groups spontaneous breathing during APRV was associated with increases (p < 0.05) in right ventricular end-diastolic volume, stroke volume, cardiac index (CI), PaO2, oxygen delivery, and mixed venous oxygen tension (PvO2) and with reductions (p < 0.05) in pulmonary vascular resistance and oxygen extraction. PSV did not consistently improve CI and PaO2 when compared with APRV without spontaneous breathing. Improved V A/Q matching during spontaneous breathing with APRV was evidenced by decreases in intrapulmonary shunt (equal Paw: 33 +/- 4 to 24 +/- 4%; equal V E: 32 +/- 4 to 25 +/- 2%) (p < 0.05), dead space (equal Paw: 44 +/- 9 to 38 +/- 6%; equal V E: 44 +/- 9 to 38 +/- 6%) (p < 0.05), and the dispersions of ventilation (equal Paw: 0.96 +/- 0.23 to 0.78 +/- 0.22; equal V E: 0.92 +/- 0.23 to 0.79 +/- 0.22) (p < 0.05), and pulmonary blood flow distribution (equal Paw: 0.89 +/- 0.12 to 0.72 +/- 0.10; equal V E: 0.94 +/- 0.19 to 0.78 +/- 0.22) (p < 0.05). PSV did not improve V A/Q distributions when compared with APRV without spontaneous breathing. These findings indicate that uncoupling of spontaneous and mechanical ventilation during APRV improves V A/Q matching in ARDS presumably by recruiting nonventilated lung units. Apparently, mechanical assistance of each inspiration during PSV is not sufficient to counteract the V A/Q maldistribution caused by alveolar collapse in patients with ARDS.

Cardiopulmonary effects of aerosolized prostaglandin E1 and nitric oxide inhalation in patients with acute respiratory distress syndrome.

Ten patients with acute respiratory distress syndrome (ARDS) received in random order nitric oxide (NO) inhalation, aerosolized prostaglandin E1 (PGE1), infusion of PGE1, or no intervention. Inhalation of either aerosolized PGE1 (10 +/- 1 ng/kg/min) or NO (7 +/- 1 ppm) reduced pulmonary vascular resistance (PVR) from 158 +/- 14 to 95 +/- 11 dyn . s/cm5/m2 (NO) and 100 +/- 12 dyn . s/cm5/m2 (aerosolized PGE1), and improved PaO2 from 78 +/- 3 to 96 +/- 5 mm Hg (NO) and 95 +/- 4 mm Hg (aerosolized PGE1) (p < 0.05), venous admixture (Q VA/Q T) from 45 +/- 2 to 36 +/- 2% (NO), and 36 +/- 2% (aerosolized PGE1) (p < 0.05), oxygen delivery (DO2) from 711 +/- 34 to 762 +/- 45 ml/min/m2 (NO) and 780 +/- 46 ml/min/m2 (aerosolized PGE1) (p < 0.05), and right ventricular ejection fraction (RVEF) from 32 +/- 6 to 37 +/- 5% (NO), and 36 +/- 4% (aerosolized PGE1) (p < 0.05) at a constant cardiac index (CI). Although infusion of PGE1 (12 +/- 1 ng/kg/min) caused a similar reduction in PVR as aerosolized PGE1 and NO inhalation, it improved RVEF and increased CI but decreased Q VA/Q T and PaO2. These results suggest that in ARDS patients inhalation of aerosolized PGE1 or NO in low concentrations equally improves PVR and gas exchange by selective vasodilation in ventilated areas.

Comparison of intubating conditions after rocuronium and suxamethonium following "rapid-sequence induction" with thiopentone in elective cases.

BACKGROUND: Rocuronium (Org 9426) was shown to have the fastest onset of action of all currently available non-depolarizing neuromuscular blocking drugs and to provide intubating conditions similar to those of suxamethonium 60 to 90 s after administration. We compared the intubating conditions after rocuronium and suxamethonium following rapid-sequence induction of anaesthesia. METHODS: Fifty unpremedicated patients of ASA physical status I or II, scheduled for elective surgery were studied. Anaesthesia was induced with thiopentone 6 mg kg-1 followed randomly by suxamethonium 1 mg kg-1 or rocuronium 0.6 mg kg-1 and, 45 s later, intubation was commenced. Muscle fasciculations, intubating conditions and intubation time, haemodynamic variables and oxygenation were assessed. RESULTS: Intubation time did not differ between suxamethonium (9.8 +/- 2.2 s) (mean +/- SD) and rocuronium (10.5 +/- 2.9 s), respectively. Intubating conditions were clinically acceptable (good or excellent) in all patients given suxamethonium and in 96% of the patients given rocuronium. However, the condition of the vocal cords was better (P < 0.05) and diaphragmatic response to intubation was less pronounced with suxamethonium (P < 0.05). Changes in heart rate and arterial blood pressure were similar in both groups. CONCLUSION: The authors conclude that rocuronium is a suitable alternative to suxamethonium for rapid tracheal intubation even under unsupplemented thiopentone anaesthesia, at least in elective, otherwise healthy patients. Its use for rapid-sequence induction under emergency conditions, however, needs further investigation.

Effect of neuromuscular blockade on the elastic properties of the lungs, thorax, and total respiratory system in anesthetized pigs.

OBJECTIVE: To evaluate the effect of neuromuscular blockade on the elastic properties of the lungs, thorax, and total respiratory system in pigs anesthetized to suppress spontaneous breathing. DESIGN: Prospective, randomized, experimental study. SETTING: A research laboratory at a university medical center. SUBJECTS: Eight healthy, anesthetized pigs, weighing 22 to 25 kg. INTERVENTIONS: Pigs, with and without muscular blockade, were mechanically ventilated during an infusion of sodium pentobarbital that was titrated to suppress spontaneous breathing activity. MEASUREMENTS AND MAIN RESULTS: No significant differences were observed between pressure/volume curves of the lungs, the chest wall, and the total respiratory system, as determined by inflating and deflating the lungs during anesthesia, with or without neuromuscular blockade, in random order. Functional residual capacity was 985 +/- 87 mL with neuromuscular blockade and 997 +/- 78 mL without neuromuscular blockade (NS). A comparison of the total respiratory system, lung, and chest wall compliances obtained with and without neuromuscular blockade showed high correlations (total respiratory system compliance [r2 = .86]; chest wall compliance [r2 = .83]). CONCLUSION: Neuromuscular blockade does not alter the elastic properties of the lungs, chest wall, or total respiratory system in mechanically ventilated pigs receiving sodium pentobarbital anesthesia to suppress spontaneous breathing efforts.

Timing of pressure release affects power of breathing and minute ventilation during airway pressure release ventilation.

OBJECTIVES: To evaluate the effects of interference between spontaneous and mechanical breaths on the power of breathing (rate at which work is done) and ventilatory support during airway pressure release ventilation. DESIGN: Multitrial tests under simulated clinical conditions using a mechanical respiratory system model. SETTING: A research laboratory at a university medical center. INTERVENTIONS: Simulated spontaneous breathing augmented with continuous positive airway pressure and airway pressure release ventilation. Variation in synchrony between spontaneous breathing and mechanical ventilation was accomplished by adjusting the time lag between detection of the spontaneous inspiration and the airway pressure release from 0 to 3 secs in increments of 0.25 secs. MEASUREMENTS AND MAIN RESULTS: Pressures and volumes were measured at the inlet of the lung and chest wall compartment of the respiratory system model. Pressure and volume changes measured at the inlet of the chest wall compartment were used to generate pressure/volume loops and to calculate the power of the spontaneous breathing. Minute ventilation was greater (p < .01) during all airway pressure release ventilation settings compared with those values of continuous positive airway pressure. Nonconflicting airway pressure release ventilation was associated with a higher minute ventilation (p < .001) than asynchronous airway pressure release ventilation. When spontaneous inspiration was synchronous with restoration of continuous positive airway pressure, minute ventilation was lower (p < .001) than during nonconflicting airway pressure release ventilation settings. Power of spontaneous breathing was highest when airway pressure release and spontaneous inspiration coincided, and lowest when spontaneous inspiration and restoration of continuous positive airway pressure were synchronized. Power of breathing was significantly lower during nonconflicting than during asynchronous airway pressure release ventilation (p < .01). No difference was observed between the power of spontaneous breathing and airway pressure release ventilation either with spontaneous expiration synchronized with airway pressure release or with nonconflicting airway pressure release ventilation. When calculated per liter of ventilation, power of spontaneous breathing was significantly lower (p < .01) during all airway pressure release ventilation settings compared with continuous positive airway pressure. CONCLUSION: Asynchronous airway pressure release may increase the power of spontaneous breathing and reduce effective mechanical ventilatory support during airway pressure release ventilation. A clinical study is required to assess the effect of synchronous and asynchronous interference between spontaneous and mechanical breaths during airway pressure release ventilation.

Subglottic positive end-expiratory pressure in extubated patients recovering from acute lung injury.

OBJECTIVE: To examine the glottic function in extubated patients recovering from acute lung injury by simultaneous measurement of airway opening and subglottic airway pressures while patients are breathing at ambient pressure and receiving continuous positive airway pressure by a face mask. DESIGN: Descriptive, prospective study. SETTING: Intensive care unit at a university hospital. PATIENTS: Ten patients who required continuous positive airway pressure of at least 7 cm H2O in order to restore gas exchange after mechanical ventilation for acute lung injury. INTERVENTIONS: Spontaneous breathing at ambient airway pressure and with continuous positive airway pressures of 5 and 10 cm H2O via face mask. MEASUREMENTS AND MAIN RESULTS: Intratracheal pressure, airway opening pressure, and airflow at the airway opening were measured. Breathing at ambient pressure resulted in significantly higher end-expiratory intratracheal pressure than end-expiratory airway opening pressure (p < .01). No significant differences between end-expiratory intratracheal pressure and end-expiratory airway opening pressure were observed during breathing with continuous positive airway pressures of 5 and 10 cm H2O. A significant end-expiratory airflow at the airway opening (p < .01), observed during ambient pressure breathing, was not detectable while the patient received mask continuous positive airway pressure. The partial pressure of oxygen in the arterial blood (Pao2) increased significantly while patients breathed with 10 cm H2O, but not while patients breathed 5 cm H2O continuous positive airway pressure compared with breathing at ambient pressure (p < .05). CONCLUSIONS: Our data imply that patients recovering from acute lung injury create an intratracheal positive end-expiratory pressure by braking the expiratory airflow, probably by glottic narrowing. Despite compensatory glottic narrowing, extubated patients with reduced lung function may benefit from higher levels of continuous positive airway pressure.

Plasma lignocaine concentrations associated with extradural analgesia in patients with and without multiple organ failure.

We have measured plasma concentrations of lignocaine after thoracic extradural analgesia with continuous infusion of lignocaine in eight intensive care patients with chest wall trauma or after major upper abdominal surgery. Four patients developed multiple organ failure (MOF). Plasma concentrations of lignocaine in arterial blood were measured 4, 8, 24 and 48 h after a continuous infusion of lignocaine was commenced in the extradural space. Plasma concentrations of lignocaine were greater in all patients with MOF (range 2.7-5.1 micrograms ml-1) than in patients without MOF (range 0.8-1.2 micrograms ml-1). Because plasma concentrations in patients with MOF were within the low toxic range, extradural infusion of lignocaine should only be considered in intensive care patients without MOF or when plasma concentrations of lignocaine are monitored.

Comparison of postoperative respiratory function after laparoscopy or open laparotomy for cholecystectomy.

Cholecystectomy performed via laparotomy is associated with reduction of lung volumes including functional residual capacity that may lead to postoperative hypoxia and atelectasis. Laparoscopic cholecystectomy is associated with faster recovery compared to open laparotomy and cholecystectomy. To determine whether laparoscopic cholecystectomy was associated with less pulmonary dysfunction, 20 patients (ASA Physical Status I) undergoing elective cholecystectomy were randomly assigned to surgical teams performing either laparoscopy or open laparotomy for cholecystectomy. Patients in whom one or the other surgical technique had to be performed for medical or psychologic indications were excluded from the study. A standardized anesthetic technique and postoperative analgesic regimen were used. Forced vital capacity and forced expiratory volume in 1 s; functional residual capacity determined by a closed-circuit, constant volume helium dilution technique; and arterial O2 and CO2 tensions were measured preoperatively and at 6, 24, and 72 h postcholecystectomy. Forced vital capacity and forced expiratory volume in 1 s were significantly greater (P less than 0.05) in the laparoscopy compared to the laparotomy group at 6, 24, and 72 h postoperatively. Forced vital capacity relative to preoperative values was significantly (P less than 0.05) greater in patients with laparoscopy (24 h, 70 +/- 14%; 72 h, 91 +/- 6%) compared to open laparotomy (24 h, 57 +/- 23%; 72 h, 77 +/- 14%). Similarly, forced expiratory volumes in 1 s relative to preoperative values were significantly (P less than 0.05) greater in patients with laparoscopy (24 h, 85 +/- 13%; 72 h, 92 +/- 9%) compared to open laparotomy (24 h, 54 +/- 22%; 72 h, 77 +/- 11%).(ABSTRACT TRUNCATED AT 250 WORDS)

Assessment of changes in lung microvascular permeability in posttraumatic acute lung failure after direct and indirect injuries to lungs.

We prospectively studied the variation in sequence of occurrence of lung microvascular permeability (LMVP) increase and clinical onset of posttraumatic acute lung failure (ALF) in the sequential failure of organ systems after direct and indirect lung injury. Acute lung failure developed in 52 of 255 trauma patients. Thirty-seven of these developed ALF after a direct injury to lung tissue and 11 after an indirect injury. Lung microvascular permeability was measured with a gamma camera simultaneously over both lungs using indium 113m-labeled transferrin and technetium 99m-labeled erythrocytes in 24 patients with ALF due to direct lung injury and in 4 with ALF due to indirect injury. A localized increased LMVP was observed initially only in the directly traumatized lung (traumatized/nontraumatized lung: 10.03 +/- 5.08/3.73 +/- 3.33 %/h), but involved the primarily nontraumatized lung within 4 days (traumatized/nontraumatized lung: 9.13 +/- 4.49/10.89 +/- 5.05 %/h). In contrast, in ALF due to indirect lung injury, an increased LMVP over both lungs was observed initially (right/left lung: 11.57 +/- 6.18/12.63 +/- 5.73 %/h) and 4 days later (right/left lung: 12.3 +/- 5.49/11.92 +/- 5.75 %/h). Acute lung failure due to direct lung injury occurred significantly earlier (less than 72 h) (P less than 0.01), whereas onset of indirectly induced ALF was later (greater than 72 h). Sepsis syndrome and multiple organ failure were the major complications once ALF occurred after a direct injury. In contrast, sepsis syndrome and multiple organ failure commonly preceded or paralleled the onset of ALF due to an indirect injury.(ABSTRACT TRUNCATED AT 250 WORDS)

[Acute lung failure following thoracic trauma]. / Das akute Lungenversagen nach Thoraxtrauma.

Pulmonary failure is almost always present in the early or late phase of multiple organ failure (MOF). Acute lung failure (ALF) is a uniquely constant response to direct or indirect insults to the lung. Increased pulmonary microvascular permeability (PMVP) is associated with the onset of lung permeability edema, the hallmark of ALF. The sequence of PMVP and the development of ALF caused by direct insults are studied. METHODS. A series of 255 trauma patients admitted to our intensive care unit (ICU) from 1987 to 1988 were enrolled in this prospective study. ALF was defined as stage III of the Posttraumatic Pulmonary Insufficiency Score; sepsis syndrome, according to Montgomery; organ failure, as stage II of the MOF score, and MOF was recorded when at least two organs had failed. Thoracic injury and aspiration were expected as direct, sepsis and shock alone as indirect insults to the lung. A computerized large field of view gamma camera was used to measure PMVP simultaneously over both lungs by means of 113mIn-transferrin and 99mTc-erythrocytes. The pulmonary microvascular permeability index (PMVPI; %/h) was used to quantify PMVP in the dynamic scintigraphic measurement. RESULTS. Of the 255 trauma patients (ISS = 33.9 +/- 18.7), 21% (52) patients (ISS = 41 +/- 17.8) developed ALF. 50 (or 96%) of the ALF patients developed MOF in addition, and 27 (72%) of the patients with directly induced ALF developed sepsis syndrome later. Direct lung injury was present in 77% (37) of the patients with posttraumatic ALF. Thoracic injury was the main cause of ALF: 58% (30) of 52 patients with ALF had a thoracic injury, which was true of only 30% of the non-ALF group (P less than 0.05). 33 (or 89%) of the ALF patients with direct injury developed ALF less than 72 h after injury (early ALF), and only 11% (4) later than 72 h after injury (late ALF). Indirect injury of the lung was present in 22% (12) of the patients with posttraumatic ALF. Indirectly induced ALF occurred in less than 72 h in 36% (4) and more than 72 h after injury in 64% (7) trauma patients. PMVP was determined in 21 of the 30 patients with thoracic injury. Initial evaluation of these patients with direct induced ALF showed significantly elevated (P less than 0.01) PMVP for the traumatized (PMVPI = 10.8 +/- 5.1%/h) but normal values for the nontraumatized lung (PMVPI = 3.9 +/- 3.4%/h), whereas 4 days later the PMVP increased significantly (P less than 0.05) on the primarily healthy side (PMVPI = 8.0 +/- 5.0%/h) while remaining elevated for the traumatized lung (PMVPI = 10.9 +/- 6.0%/h). In the control group the PMVPI was 2.6 +/- 2.8%/h for the right and 2.0 +/- 2.8%/h for the left lung. Similar values were found in mechanically ventilated ICU patients without ALF. DISCUSSION. Direct injury seems to be the dominant mechanism for early manifestation (less than 72 h) of posttraumatic ALF. The thoracic trauma seems to damage the pulmonary endothelium directly, thus increasing PMVP in a circumscribed region. An overwhelming inflammatory response may cause the later increase in PMVP in the primarily healthy lung areas.