Is maximal lung recruitment worth it?
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Publications and source records attributed to Alejandro Bruhn.
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BACKGROUND: Recent studies have suggested that strict glucose control with intensive insulin therapy in critically ill patients may result in better outcomes. Whether this is also true in septic shock has not been determined. In addition, whether it is the insulin administration per se or the glucose control that contributes to the beneficial effects is unclear. We raised the hypothesis that euglycemic hyperinsulinemia (EH) might improve the outcome from septic shock due to peritonitis. MATERIALS AND METHODS: Fourteen anesthetized, mechanically ventilated, and hemodynamically monitored sheep received 1.5 g/kg body weight i.p. feces to induce sepsis. Ringer's lactate and 6% hydroxyethyl starch solutions were infused throughout the experiment to prevent hypovolemia. Two hours after feces injection, the animals were randomized to either an EH group (n = 7) receiving insulin 0.25 U/ kg/h, 20% glucose (to maintain blood glucose at 40-90 mg/dl), and potassium (to maintain the potassium level at 4.0- 5.5 mmol/l) or a control group (n = 7) with no intervention. All animals were studied until their spontaneous death or for 30 h. RESULTS: The EH group received a greater volume of 20% glucose, but blood glucose and potassium concentrations were similar in the two groups. No significant differences were found in hemodynamic variables. The circulating interleukin-6 levels increased in both groups after feces injection, but tended to be lower in the EH group (p < 0.05). The survival times were similar in the two groups (median 20.0 h in the EH group vs. 17.0 h in the control group; p = 0.73). CONCLUSIONS: In this clinically relevant sheep septic shock model, EH decreased blood interleukin-6 concentrations but did not change hemodynamics or improve the outcome.
OBJECTIVE: Alkaline phosphatase may decrease the harmful effects of lipopolysaccharide by detoxifying lipid A. The aim of this study was to investigate whether administration of alkaline phosphatase is beneficial in a clinically relevant septic shock model. DESIGN: Interventional laboratory study. SETTING: University hospital animal research laboratory. SUBJECTS: Fourteen fasted, anesthetized, invasively monitored, mechanically ventilated, female sheep (27.6 +/- 3.9 kg). INTERVENTIONS: Each animal received 1.5 g/kg body weight of feces intraperitoneally to induce sepsis. Ringer's lactate and a 6% hydroxyethyl starch solution were infused throughout the experiment to prevent hypovolemia. Two hours after feces injection, animals were randomized to alkaline phosphatase (60 units/kg intravenous bolus followed by a continuous infusion of 20 units/kg/hr for a total of 15 hrs) or no alkaline phosphatase (control group). MEASUREMENTS AND MAIN RESULTS: All animals were studied until their spontaneous death or for a maximum of 30 hrs. Plasma alkaline phosphatase concentrations decreased in the control group but increased in the treatment group following alkaline phosphatase administration. In the treatment group, the Pao2/Fio2 ratio was higher (p < .05), blood interleukin-6 concentrations were lower (p < .05), and the survival time was longer (median time 23.8 vs. 17 .0 hrs, p < 0.05) than in the control group. There were no significant differences in systemic hemodynamics or diuresis. CONCLUSIONS: In this clinically relevant septic shock model, alkaline phosphatase administration improved gas exchange, decreased interleukin-6 concentrations, and prolonged survival time.
Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that plays a major role in the pathogenesis of sepsis. Some studies have indicated that glucocorticoids increase MIF production in physiological conditions. The goal of this study was to determine whether glucocorticoid treatment also upregulates MIF production in sepsis. Male NMRI mice (6-10 weeks old) underwent laparotomy, proximal ligation of the cecum, and double perforation with a 19-gauge needle (cecal ligation and puncture). Mice were randomly treated with saline (control) or dexamethasone at doses of 0.1, 1, or 10 mg/kg ip. At 6 or 18 h postoperatively, 10 mice per group were euthanized; and blood, peritoneal fluid, liver, lung, kidney, and heart tissue samples were retrieved. MIF, IL-6, TNF-alpha, and IL-10 were measured by enzyme-linked immunosorbent assay. Sepsis induced by cecal ligation and puncture produced a marked increase in MIF and cytokine levels in plasma and peritoneal fluid. Treatment with dexamethasone 10 mg/kg decreased MIF levels in plasma after 18 h, but there was no effect of dexamethasone on MIF production locally in the peritoneal cavity or in the liver, lungs, heart, or kidneys. We conclude that glucocorticoid treatment does not upregulate MIF production in sepsis.
BACKGROUND: The subject of the best vasopressor for hemodynamic management of septic shock (SS) is controversial. One of the difficulties in planning such studies is that physicians are reluctant to use one vasopressor exclusively, and there is considerable variation in practice. The aim of this study was to test the feasibility of implementing a single pressor-based algorithm (in this case, norepinephrine [NE]). METHODS: A NE-based algorithm was applied prospectively to 100 consecutive SS patients. A formal training program was implemented before starting the protocol and applied to 72 physicians and nurses involved in intensive care unit (ICU) patient care. Compliance, protocol violations, probable adverse effects, and outcome were evaluated on a daily basis by an independent group of fellows and a research nurse. RESULTS: In 100 patients, there were 7,139 hours of algorithm use. Only 13 protocol violations were observed, mostly in the timing of inotropic drugs. Senior staff physicians or busy night shifts accounted for most of these violations. ICU mortality was 33%, which is comparable to that predicted by Acute Physiology and Chronic Health Evaluation II and Sequential Organ Failure Assessment scores. Adverse events probably related to NE were not observed. CONCLUSIONS: The present algorithm, applied after a strict training program, obtained an overall good acceptance and compliance with very few protocol violations in more than 7,000 hours of use. Safety was demonstrated by a global mortality comparable to that predicted by severity scores and absence of specific drug-related morbidity. The implementation of a single pressor-based algorithm for SS is feasible and safe.
UNLABELLED: Management of septic shock (SS) with a norepinephrine (noradrenaline)-based haemodynamic algorithm. INTRODUCTION: The choice of the best vasopressor for haemodynamic management of septic shock is controversial. Nevertheless, very few studies have been focused on evaluating different management algorithms. The aim of this study was to evaluate the performance of a norepinephrine (NE)-based management protocol. Experience with NE as the initial vasopressor, even if not comparative, could bring relevant data for planning future trails. We also wanted to evaluate the compliance of critical care physicians and nurses with haemodynamic management protocol. PATIENTS AND METHOD: A norepinephrine-based algorithm for the management of septic shock that commands different sequential interventions according to its requirements, was applied prospectively to 100 consecutive septic shock patients. RESULTS: Norepinephrine was used as the first vasoactive drug in all patients with a maximum dose of 0.31+/-0.3 microg kg(-1)min(-1) and an ICU mortality of 33%. Physicians applied correctly all the steps of the algorithm in 92% of the patients. Applying the algorithm, avoided the use of pulmonary artery catheter in 31 patients and led to use of lower doses of vasoactive agents than in many other clinical experiences. CONCLUSION: In conclusion, our data support extended use of an algorithm based on norepinephrine for treating septic shock patients. This is the first clinical study that uses NE as the initial vasopressor drug systematically, and although not comparative, the mortality rates adjusted to APACHE II, are comparable to other studies. It also gives support for future clinical trials comparing norepinephrine with dopamine in this setting.
INTRODUCTION: Positive end-expiratory pressure (PEEP) improves oxygenation and can prevent ventilator-induced lung injury in patients with acute respiratory distress syndrome (ARDS). Nevertheless, PEEP can also induce detrimental effects by its influence on the cardiovascular system. The purpose of this study was to assess the effects of PEEP on gastric mucosal perfusion while applying a protective ventilatory strategy in patients with ARDS. METHODS: Eight patients were included. A pressure-volume curve was traced and ideal PEEP, defined as lower inflection point + 2 cmH2O, was determined. Gastric tonometry was measured continuously (Tonocap). After baseline measurements, 10, 15 and 20 cmH2O PEEP and ideal PEEP were applied for 30 min each. By the end of each period, hemodynamic, CO2 gap (gastric minus arterial partial pressures), and ventilatory measurements were performed. RESULTS: PEEP had no effect on CO2 gap (median [range], baseline: 19 [2-30] mmHg; PEEP 10: 19 [0-40] mmHg; PEEP 15: 18 [0-39] mmHg; PEEP 20: 17 [4-39] mmHg; ideal PEEP: 19 [9-39] mmHg; P = 0.18). Cardiac index also remained unchanged (baseline: 4.6 [2.5-6.3] l min(-1) m(-2); PEEP 10: 4.5 [2.5-6.9] l min(-1) m(-2); PEEP 15: 4.3 [2-6.8] l min(-1) m(-2); PEEP 20: 4.7 [2.4-6.2] l min(-1) m(-2); ideal PEEP: 5.1 [2.1-6.3] l min(-1) m(-2); P = 0.08). One patient did not complete the protocol because of hypotension. CONCLUSION: PEEP of 10-20 cmH2O does not affect gastric mucosal perfusion and is hemodynamically well tolerated in most patients with ARDS, including those receiving adrenergic drugs.
OBJECTIVE: To assess the acute effect of a lung recruitment maneuver (LRM) on lung morphology in patients with acute lung injury (ALI) or acute respiratory distress syndrome (ARDS). PATIENTS: Ten patients with ALI/ARDS on mechanical ventilation. DESIGN: Prospective clinical study. SETTING: Computed tomography (CT) scan facility in a teaching hospital. INTERVENTIONS: An LRM performed by stepwise increases in positive end-expiratory pressure (PEEP) of up to 30-40 cm H(2)O. Lung basal CT sections were taken at end-expiration (patients 1 to 5), and at end-expiration and end-inspiration (patients 6 to 10). Arterial blood gases and static compliance (C(st)) were measured before, during and after the LRM. MEASUREMENTS AND MAIN RESULTS: Poorly aerated and non-aerated tissue at PEEP 10 cm H(2)O accounted for 60.0+/-29.1% of lung parenchyma, while only 1.1+/-1.8% was hyperinflated. Increasing PEEP to 20 and 30 cm H(2)O, compared to PEEP 10 cm H(2)O, decreased poorly aerated and non-aerated tissue by 16.2+/-28.0% and 33.4+/-13.8%, respectively ( p<0.05). This was associated with an increase in PaO(2) and a decrease in total static compliance. Inspiration increased alveolar recruitment at all PEEP levels. Hyperinflated tissue increased up to 2.9+/-4.0% with PEEP 30 cm H(2)O, and to a lesser degree with inspiration. No barotrauma or severe hypotension occurred. CONCLUSIONS: Lung recruitment maneuvers improve oxygenation by expanding collapsed alveoli without inducing too much hyperinflation in ALI/ARDS patients. An LRM during the CT scan gives morphologic and functional information that could be useful in setting ventilatory parameters.
Lung computed tomography (CT) is being used increasingly to assess lung morphology in patients on mechanical ventilation. Lung CT under known levels of airway pressure (dynamic CT) can also assess the response of lung parenchyma to ventilatory therapy. We report a patient with acute respiratory distress syndrome secondary to descending necrotizing mediastinitis, in whom lung dynamic CT oriented ventilatory management. Independent lung ventilation improved gas exchange and helped patient recovery.