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John G Laffey

Publications and source records attributed to John G Laffey.

16 recordsLinked to original sources
PubMed2007

The analgesic efficacy of transversus abdominis plane block after abdominal surgery: a prospective randomized controlled trial.

BACKGROUND: The transversus abdominis plane (TAP) block is a novel approach for blocking the abdominal wall neural afferents via the bilateral lumbar triangles of Petit. We evaluated its analgesic efficacy in patients during the first 24 postoperative hours after abdominal surgery, in a randomized, controlled, double-blind clinical trial. METHODS: Thirty-two adults undergoing large bowel resection via a midline abdominal incision were randomized to receive standard care, including patient-controlled morphine analgesia and regular nonsteroidal antiinflammatory drugs and acetaminophen (n = 16), or to undergo TAP block (n = 16) in addition to standard care (n = 16). After induction of anesthesia, 20 mL of 0.375% levobupivacaine was deposited into the transversus abdominis neuro-fascial plane via the bilateral lumbar triangles of Petit. Each patient was assessed by a blinded investigator in the postanesthesia care unit and at 2, 4, 6, and 24 h postoperatively. RESULTS: The TAP block reduced visual analog scale pain scores (TAP versus control, mean +/- sd) on emergence (1 +/- 1.4 vs 6.6 +/- 2.8, P < 0.05), and at all postoperative time points, including at 24 h (1.7 +/- 1.7 vs 3.1 +/- 1.5, P < 0.05). Morphine requirements in the first 24 postoperative hours were also reduced (21.9 +/- 8.9 mg vs 80.4 +/- 19.2 mg, P < 0.05). There were no complications attributable to the TAP block. All TAP patients reported high levels of satisfaction with their postoperative analgesic regimen. CONCLUSIONS: The TAP block provided highly effective postoperative analgesia in the first 24 postoperative hours after major abdominal surgery.

Abdomen↗
PubMed2006

Tracheal intubation by inexperienced medical residents using the Airtraq and Macintosh laryngoscopes--a manikin study.

The Airtraq laryngoscope is a novel intubation device that may possess advantages over conventional direct laryngoscopes for use by personnel that are infrequently required to perform tracheal intubation. We conducted a prospective study in 20 medical residents with little prior airway management experience. After brief didactic instruction, each participant took turns performing laryngoscopy and intubation using the Macintosh (Welch Allyn, Welch Allyn, NY) and Airtraq (Prodol Ltd. Vizcaya, Spain) devices, in 3 laryngoscopy scenarios in a Laerdal Intubation Trainer (Laerdal, Stavanger, Norway) and 1 scenario in a Laerdal SimMan manikin (Laerdal, Kent, UK). They then performed tracheal intubation of the normal airway a second time to characterize the learning curve. In all scenarios tested, the Airtraq decreased the duration of intubation attempts, reduced the number of optimization maneuvers required, and reduced the potential for dental trauma. The residents found the Airtraq easier to use in all scenarios compared with the Macintosh laryngoscope. The Airtraq may constitute a superior device for use by personnel infrequently required to perform tracheal intubation.

Clinical Competence↗
PubMed2005

Permissive hypercapnia: role in protective lung ventilatory strategies.

PURPOSE OF REVIEW: Hypercapnia is a central component of current protective ventilatory strategies. This review aims to present and interpret data from recent clinical and experimental studies relating to hypercapnia and its role in protective ventilatory strategies. RECENT FINDINGS: Increasing clinical evidence supports the use of permissive hypercapnia, particularly in acute lung injury/acute respiratory distress syndrome, status asthmaticus, and neonatal respiratory failure. However, there are no clinical data examining the contribution of hypercapnia per se to protective ventilatory strategies. Recent experimental studies provide further support for the concept of therapeutic hypercapnia, whereby deliberately elevated PaCO2 may attenuate lung and systemic organ injury. CO2 administration attenuates experimental acute lung injury because of adverse ventilatory strategies, mesenteric ischemia reperfusion, and pulmonary endotoxin instillation. Hypercapnic acidosis attenuates key effectors of the inflammatory response and reduces lung neutrophil infiltration. At the genomic level, hypercapnic acidosis attenuates the activation of nuclear factor-kappaB, a key regulator of the expression of multiple genes involved in the inflammatory response. The physiologic effects of hypercapnia, both beneficial and potentially deleterious, are increasingly well understood. In addition, reports suggest that humans can tolerate extreme levels of hypercapnia for relatively prolonged periods without adverse effects. SUMMARY: The potential for hypercapnia to contribute to the beneficial effects of protective lung ventilatory strategies is clear from experimental studies. However, the optimal ventilatory strategy and the precise contribution of hypercapnia to this strategy remain unclear. A clearer understanding of its effects and mechanisms of action is central to determining the safety and therapeutic utility of hypercapnia in protective lung ventilatory strategies.

Acidosis↗
PubMed2005

Hypercapnic acidosis does not modulate the severity of bacterial pneumonia-induced lung injury.

OBJECTIVE: Deliberate induction of hypercapnic acidosis protects against lung injury after ischemia-reperfusion, endotoxin-induced, and ventilation-induced lung injury. The efficacy of hypercapnic acidosis in bacterial lung infection, a common cause of acute respiratory distress syndrome, is not known. Furthermore, its effect may differ depending on the presence or absence of antibiotic therapy. We investigated whether hypercapnic acidosis-induced by adding CO2 to inspired gas-would protect against acute lung injury induced by pulmonary Escherichia coli instillation in an in vivo model in the presence and absence of effective antibiotic therapy. DESIGN: Prospective randomized animal study. SETTING: University research laboratory. SUBJECTS: Adult male Wistar-Kyoto rats. INTERVENTIONS: The animals were anesthetized and ventilated. In series 1, rats were administered intravenous ceftriaxone (100 mg x kg) and randomized to normocapnia (Normocapnia-ABx; Fico2 0.00, n = 10) or hypercapnia (Hypercapnia-ABx; Fico2 0.05, n = 10) groups. E. coli (8.4 x 10 colony forming units) was instilled intratracheally. Series 2 animals did not receive antibiotics. They were randomized to normocapnia (Normocapnia, n = 10) or hypercapnia (Hypercapnia, n = 10) groups, and intratracheal E. coli was administered. All animals were ventilated for 6 hrs. MEASUREMENTS AND MAIN RESULTS: In series 1, there were no differences between Hypercapnia-ABx and Normocapnia-ABx groups with regard to: (a-a)o2 gradient (mean +/- sem; 215 +/- 13 vs. 252 +/- 22 mm Hg), Pao2, bronchoalveolar lavage neutrophil count, static lung compliance, or histologic injury. Lung bacterial yield was not different between the groups. In series 2, in the absence of antibiotic therapy, there were no differences between Hypercapnia and Normocapnia groups in: (a-a)o2 gradient (mean +/- sem, 345 +/- 25 vs. 332 +/- 23 mm Hg), systemic Pao2, bronchoalveolar lavage neutrophil count, or static lung compliance. Lung bacterial yield was not altered by hypercapnia in either series 1 or 2. CONCLUSIONS: We conclude that hypercapnic acidosis did not alter the magnitude of the lung injury induced by intratracheal E. coli instillation in the presence or absence of antibiotics.

Acidosis, Respiratory↗
PubMed2005

Maternal brain death and somatic support.

Brain death is a concept used in situations in which life-support equipment obscures the conventional cardiopulmonary criteria of death, and it is legally recognized in most countries worldwide. Brain death during pregnancy is an occasional and tragic occurrence. The mother and fetus are two distinct organisms, and the death of the mother mandates consideration of the well-being of the fetus. Where maternal brain death occurs after the onset of fetal viability, the benefits of prolonging the pregnancy to allow further fetal maturation must be weighed against the risks of continued time in utero, and preparations must be made to facilitate urgent cesarean section and fetal resuscitation at short notice. Where the fetus is nonviable, one must consider whether continuation of maternal organ supportive measures in an attempt to attain fetal viability is appropriate, or whether it constitutes futile care. Although the gestational age of the fetus is central to resolving this issue, there is no clear upper physiological limit to the prolongation of somatic function after brain death. Furthermore, medical experience regarding prolonged somatic support is limited and can be considered experimental therapy. This article explores these issues by considering the concept of brain death and how it relates to somatic death. The current limits of fetal viability are then discussed. The complex ethical issues and the important variations in the legal context worldwide are considered. Finally, the likelihood of successfully sustaining maternal somatic function for prolonged periods and the medical and obstetric issues that are likely to arise are examined.

Abortion, Therapeutic↗
PubMed2004

Bench-to-bedside review: Permissive hypercapnia.

Current protective lung ventilation strategies commonly involve hypercapnia. This approach has resulted in an increase in the clinical acceptability of elevated carbon dioxide tension, with hypoventilation and hypercapnia 'permitted' in order to avoid the deleterious effects of high lung stretch. Advances in our understanding of the biology of hypercapnia have prompted consideration of the potential for hypercapnia to play an active role in the pathogenesis of inflammation and tissue injury. In fact, hypercapnia may protect against lung and systemic organ injury independently of ventilator strategy. However, there are no clinical data evaluating the direct effects of hypercapnia per se in acute lung injury. This article reviews the current clinical status of permissive hypercapnia, discusses insights gained to date from basic scientific studies of hypercapnia and acidosis, identifies key unresolved concerns regarding hypercapnia, and considers the potential clinical implications for the management of patients with acute lung injury.

Acidosis↗
PubMed2004

Maternal brain death: medical, ethical and legal issues.

CASE PRESENTATION: We present the case of a pregnant woman who experienced a cerebral venous sinus thrombosis resulting in brain death at 13 weeks gestation. We discuss the management of the mother and foetus following this tragic event. We also discuss the complex medical, legal and ethical issues that arose following maternal brain death. The central question is whether continuing maternal organ supportive measures in an attempt to prolong gestation to attain foetal viability is appropriate, or whether it constitutes futile care. DISCUSSION: Successful maintenance of maternal brain somatic function to facilitate foetal maturation in utero has been reported. While the gestational age of the foetus is central to resolving this issue, there is no clear upper physiological limit to the prolongation of somatic function following brain death. Furthermore, medical experience regarding prolonged somatic support is limited. Finally, the legal rights conferred on the foetus may vary significantly depending on the jurisdiction in which the maternal brain death occurs and may have important implications. CONCLUSIONS: A consensus building approach, involving the family, is essential to resolving these potentially conflicting issues.

Adult↗
PubMed2004

Permissive hypercapnia--role in protective lung ventilatory strategies.

"Permissive hypercapnia" is an inherent element of accepted protective lung ventilation. However, there are no clinical data evaluating the efficacy of hypercapnia per se, independent of ventilator strategy. In the absence of such data, it is necessary to determine whether the potential exists for an active role for hypercapnia, distinct from the demonstrated benefits of reduced lung stretch. In this review, we consider four key issues. First, we consider the evidence that protective lung ventilatory strategies improve survival and we explore current paradigms regarding the mechanisms underlying these effects. Second, we examine whether hypercapnic acidosis may have effects that are additive to the effects of protective ventilation. Third, we consider whether direct elevation of CO(2), in the absence of protective ventilation, is beneficial or deleterious. Fourth, we address the current evidence regarding the buffering of hypercapnic acidosis in ARDS. These perspectives reveal that the potential exists for hypercapnia to exert beneficial effects in the clinical context. Direct administration of CO(2) is protective in multiple models of acute lung and systemic injury. Nevertheless, several specific concerns remain regarding the safety of hypercapnia. At present, protective ventilatory strategies that involve hypercapnia are clinically acceptable, provided the clinician is primarily targeting reduced tidal stretch. There are insufficient clinical data to suggest that hypercapnia per se should be independently induced, nor do outcome data exist to support the practice of buffering hypercapnic acidosis. Rapidly advancing basic scientific investigations should better delineate the advantages, disadvantages, and optimal use of hypercapnia in ARDS.

Acidosis, Respiratory↗
PubMed2004

New strategies to control the inflammatory response in cardiac surgery.

PURPOSE OF REVIEW: To present and interpret data from recent clinical studies (July 2002-August 2003) of strategies to control the inflammatory response after cardiac surgery. RECENT FINDINGS: Off-pump coronary artery bypass techniques, which avoid the need for extracorporeal circulation, attenuate the inflammatory response and appear to confer clinical benefit. Concerns regarding the quality of the revascularization after off-pump coronary artery bypass appear to have been allayed. At present, ventricular assist devices do not enhance the efficacy of off-pump coronary artery bypass. In patients undergoing cardiopulmonary bypass, heparin-coated circuits, hypothermic pulmonary perfusion, normoxic reperfusion after aortic unclamping, and modified ultrafiltration hold promise. Strategies to maintain perioperative haemodynamic stability, such as enoximone therapy, may be beneficial, particularly in elderly patients. Aprotinin may have important beneficial anti-inflammatory actions in higher-risk adult and paediatric patients. The therapeutic potential of corticosteroids, particularly when administered in multiple dosages is increasingly clear. Direct anti-mediator therapies that focus upon key effector molecules and pathways of the inflammatory response offer future therapeutic options. SUMMARY: The potential for strategies that inhibit the inflammatory response to improve outcome after cardiac surgery is clear. Large-scale multicentre trials investigating the most promising strategies, including off-pump coronary artery bypass, heparin-coated circuits, and perioperative corticosteroid and aprotinin therapy, are urgently needed. These trials need to be restricted to the high-risk patient groups most likely to experience benefit. In the interim, the optimal strategy to minimize the inflammatory response to cardiac surgery will remain elusive.

Journal Article↗
PubMed2003

Effects of therapeutic hypercapnia on mesenteric ischemia-reperfusion injury.

Hypercapnic acidosis protects against direct lung injury in in vivo and ex vivo models, however, lung injury/acute respiratory distress syndrome commonly occurs after a nonpulmonary etiology. We investigated whether therapeutic hypercapnia (TH)-deliberate elevation of carbon dioxide (CO2) tension-would protect against lung injury after splanchnic ischemia-reperfusion injury in an in vivo model. TH was associated with preservation of lung mechanics, attenuation of protein leakage, and improved oxygenation compared with control conditions. Lung protection was therapeutic as well as prophylactic. Protection was dose-dependent, but inspired CO2 concentrations above 5.0% were associated with little additional lung protection. Before lung injury, increasing FICO2 resulted in a dose-dependent increase in PaO2. Lung protection with hypercapnia occurred despite pulmonary artery pressures that were greater than observed with normocapnia. Reperfusion increased lipid peroxidation (tissue 8-isoprostane concentration) in the bowel, liver, and lung, and caused histologically apparent bowel injury; however, none of these effects was altered by TH. Therefore, TH-induced by adding CO2 to inspired gas-provides consistent protection against lung injury in terms of lung permeability, oxygenation, and lung mechanics after mesenteric ischemia-reperfusion. These data further support the emerging evidence for ongoing physiologic study of TH at the bedside.

Animals↗
PubMed2003

Therapeutic hypercapnia is not protective in the in vivo surfactant-depleted rabbit lung.

Permissive hypercapnia because of reduced tidal volume is associated with improved survival in lung injury, whereas therapeutic hypercapnia-deliberate elevation of arterial Pco2-protects against in vivo reperfusion injury and injury produced by severe lung stretch. No published studies to date have examined the effects of CO2 on in vivo models of neonatal lung injury. We used an established in vivo rabbit model of surfactant depletion to investigate whether therapeutic hypercapnia would improve oxygenation and protect against ventilator-induced lung injury. Animals were randomized to injurious (tidal volume, 12 mL/kg; positive end-expiratory pressure, 0 cm H2O) or protective ventilatory strategy (tidal volume, 5 mL/kg; positive end-expiratory pressure, 12.5 cm H2O), and to receive either control conditions or therapeutic hypercapnia (fraction of inspired CO2, 0.12). Oxygenation (alveolar-arterial O2 difference, arterial Po2), lung injury (alveolar-capillary protein leak, impairment of static compliance), and selected bronchoalveolar lavage and plasma cytokines (IL-8, growth-related oncogene, monocyte chemoattractant protein-1, and tumor necrosis factor-alpha) were measured. Injurious ventilation resulted in a large alveolar-arterial O2 gradient, elevated peak airway pressure, increased protein leak, and impaired lung compliance. Therapeutic hypercapnia did not affect any of these outcomes. Tumor necrosis factor-alpha was not increased by mechanical stretch in any of the groups. Therapeutic hypercapnia abolished the stretch-induced increase in bronchoalveolar lavage monocyte chemoattractant protein-1, but did not affect any of the other mediators studied. Therapeutic hypercapnia may attenuate the impairment in oxygenation and inhibit certain cytokines. Because hypercapnia inhibits certain cytokines but does not alter lung injury, the pathogenic role of these cytokines in lung injury is questionable.

Acid-Base Equilibrium↗
PubMed2003

Hypercapnic acidosis attenuates endotoxin-induced acute lung injury.

Deliberate induction of prophylactic hypercapnic acidosis protects against lung injury after in vivo ischemia-reperfusion and ventilation-induced lung injury. However, the efficacy of hypercapnic acidosis in sepsis, the commonest cause of clinical acute respiratory distress syndrome, is not known. We investigated whether hypercapnic acidosis--induced by adding CO2 to inspired gas--would be protective against endotoxin-induced lung injury in an in vivo rat model. Prophylactic institution of hypercapnic acidosis (i.e., induction before endotoxin instillation) attenuated the decrement in arterial oxygenation, improved lung compliance, and attenuated alveolar neutrophil infiltration compared with control conditions. Therapeutic institution of hypercapnic acidosis, that is, induction after endotoxin instillation, attenuated the decrement in oxygenation, improved lung compliance, and reduced alveolar neutrophil infiltration and histologic indices of lung injury. Therapeutic hypercapnic acidosis attenuated the endotoxin-induced increase in the higher oxides of nitrogen and nitrosothiols in the lung tissue and epithelial lining fluid. Lung epithelial lining fluid nitrotyrosine concentrations were increased with hypercapnic acidosis. We conclude that hypercapnic acidosis attenuates acute endotoxin-induced lung injury, and is efficacious both prophylactically and therapeutically. The beneficial actions of hypercapnic acidosis were not mediated by inhibition of peroxynitrite-induced nitration within proteins.

Acidosis, Respiratory↗
PubMed2003

Carbon dioxide attenuates pulmonary impairment resulting from hyperventilation.

OBJECTIVE: Deliberate elevation of PaCO2 (therapeutic hypercapnia) protects against lung injury induced by lung reperfusion and severe lung stretch. Conversely, hypocapnic alkalosis causes lung injury and worsens lung reperfusion injury. Alterations in lung surfactant may contribute to ventilator-associated lung injury. The potential for CO2 to contribute to the pathogenesis of ventilator-associated lung injury at clinically relevant tidal volumes is unknown. We hypothesized that: 1) hypocapnia would worsen ventilator-associated lung injury, 2) therapeutic hypercapnia would attenuate ventilator-associated lung injury; and 3) the mechanisms of impaired compliance would be via alteration of surfactant biochemistry. DESIGN: Randomized, prospective animal study. SETTING: Research laboratory of university-affiliated hospital. SUBJECTS: Anesthetized, male New Zealand Rabbits. INTERVENTIONS: All animals received the same ventilation strategy (tidal volume, 12 mL/kg; positive end-expiratory pressure, 0 cm H2O; rate, 42 breaths/min) and were randomized to receive FiCO2 of 0.00, 0.05, or 0.12 to produce hypocapnia, normocapnia, and hypercapnia, respectively. MEASUREMENTS AND MAIN RESULTS: Alveolar-arterial oxygen gradient was significantly lower with therapeutic hypercapnia, and peak airway pressure was significantly higher with hypocapnic alkalosis. However, neither static lung compliance nor surfactant chemistry (total surfactant, aggregates, or composition) differed among the groups. CONCLUSIONS: At clinically relevant tidal volume, CO2 modulates key physiologic indices of lung injury, including alveolar-arterial oxygen gradient and airway pressure, indicating a potential role in the pathogenesis of ventilator-associated lung injury. These effects are surfactant independent.

Animals↗
PubMed2002

Hypocapnia.

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Acid-Base Imbalance↗