Percutaneous endoscopic gastrostomy with T-bar fixation in children and infants.

BACKGROUND: The standard for placement of pediatric gastrostomy tubes has been percutaneous endoscopic gastrostomy (PEG) using the Ponsky "pull" technique. This study evaluated the safety and efficacy of PEG placement using the "push" technique with T-bar fixation in pediatric patients. This technique generally is limited to the adult population. With this technique, endoscopy is performed. The stomach is insufflated, and the anterior abdominal wall is transilluminated. T-bar fasteners are sequentially deployed to secure the stomach to the anterior abdominal wall. Using a modified Seldinger technique, a gastrostomy tube is placed through the center of the T-bars. METHODS: A retrospective review of all PEG tubes placed in pediatric patients from 1997 to 2003 using the T-bar gastroscopy "push" technique was conducted. Patients 18 years of age or younger were included in the study. Data collected included patient age, operative time, procedure location, and complications. RESULTS: The procedure was performed for 47 children (mean age, 6.4 years), including 15 infants younger than 1 year. The indications for long-term enteral access included failure to thrive (n = 11), feeding disorder secondary to neurologic dysfunction (n = 31), gastroparesis (n = 1), and dysphagia (n = 4). The operative time averaged 23 min (range, 12-45 min). One major complication occurred (gastrocolonic fistula). The one minor complication was early dislodgement of the gastrostomy tube, which required replacement. CONCLUSION: This study found the described technique to be safe and effective for the placement of gastrostomy tubes in infants and children.

Matrix metalloproteinase inhibitor prevents acute lung injury after cardiopulmonary bypass.

BACKGROUND: Acute lung injury (ALI) after cardiopulmonary bypass (CPB) results from sequential priming and activation of neutrophils. Activated neutrophils release neutral serine, elastase, and matrix metalloproteinases (MMPs) and oxygen radical species, which damage alveolar-capillary basement membranes and the extracellular matrix, resulting in an ALI clinically defined as adult respiratory distress syndrome (ARDS). We hypothesized that treatment with a potent MMP and elastase inhibitor, a chemically modified tetracycline (CMT-3), would prevent ALI in our sequential insult model of ALI after CPB. METHODS AND RESULTS: Anesthetized Yorkshire pigs were randomized to 1 of 5 groups: control (n=3); CPB (n=5), femoral-femoral hypothermic bypass for 1 hour; LPS (n=7), sham bypass followed by infusion of low-dose Escherichia coli lipopolysaccharide (LPS; 1 microgram/kg); CPB+LPS (n=6), both insults; and CPB+LPS+CMT-3 (n=5), both insults plus intravenous CMT-3 dosed to obtain a 25-micromol/L blood concentration. CPB+LPS caused severe lung injury, as demonstrated by a significant fall in PaO(2) and an increase in intrapulmonary shunt compared with all groups (P<0.05). These changes were associated with significant pulmonary infiltration of neutrophils and an increase in elastase and MMP-9 activity. CONCLUSIONS: All pathological changes typical of ALI after CPB were prevented by CMT-3. Prevention of lung dysfunction followed an attenuation of both elastase and MMP-2 activity. This study suggests that strategies to combat ARDS should target terminal neutrophil effectors.

Videomicroscopy provides accurate in vivo assessment of pulmonary microvascular reactivity in rabbits.

When defining the mechanism of hypoxic pulmonary vasoconstriction (HPV), investigators have employed ex vivo preparations because of the belief that accurate, quantitative assessment of pulmonary microvessels could not be obtained in vivo. We hypothesize that accurate, quantitative assessment of pulmonary microvascular reactivity can be performed using a simple, in vivo preparation. Our aim was to provide this quantitative assessment in a defined animal model, and to confirm that the chosen preparation could discriminate changes in microvascular reactivity as influenced by endogenous mediators. New Zealand rabbits were instrumented for in vivo microscopy and direct measurement of subpleural arterioles. Rabbits were first randomized to either control (n = 7) or endotoxin (n = 5), infusion of Escherichia coli lipopolysaccharide (200 Fg/kg). All rabbits were then exposed to a repeated protocol of normoxia (21% O2) for 20 min and then hypoxia (15% O2) for 10 min over 2 h. The changes in arteriole diameter were measured at the end of each interval. Normal pulmonary arterioles repeatedly constrict 15+/-3.5% during hypoxia. Altering endogenous vasoactive mediators, as with infusion of endotoxin, caused a loss of hypoxia-induced vasoconstriction. The results of our study validate this experimental preparation for the reliable quantification of pulmonary microvascular reactivity and investigation of hypoxic pulmonary vasoconstriction under both normal and pathologic conditions.

Invasive arterial BP monitoring in trauma and critical care: effect of variable transducer level, catheter access, and patient position.

OBJECTIVES: (1) To determine the validity of current recommendations for direct arterial BP measurement that suggest that the transducer (zeroed to atmosphere) be placed level with the catheter access regardless of subject positioning: and (2) to investigate the effect of transducer level, catheter access site, and subject positioning on direct arterial BP measurement. DESIGN: Prospective, controlled laboratory study. SETTING: Large animal laboratory. SUBJECTS: Five Yorkshire pigs. INTERVENTIONS: Anesthetized animals had 16F catheters placed at three access sites: aortic root, femoral artery, and distal hind limb. Animals were placed in supine, reverse Trendelenburg 35 degrees, and Trendelenburg 25 degrees positions with a transducer placed level to each access site while in every position. MEASUREMENTS AND MAIN RESULTS: For each transducer level, five systolic and diastolic pressures were measured and used to calculate five corresponding mean arterial pressures (MAPs) at each access site. When transducers were at the aortic root, MAP corresponding to aortic root pressure was obtained in all positions regardless of catheter access site. When transducers were moved to the level of catheter access, as current recommendations suggest, significant errors in aortic MAP occurred in the reverse Trendelenburg position. The same trend for error was noted in the Trendelenburg position but did not reach statistical significance. CONCLUSIONS: (1) Current recommendations that suggest placing the transducer at the level of catheter access regardless of patient position are invalid. Significant errors occur when subjects are in nonsupine positions. (2) Valid determination of direct arterial BP is dependent only on transducer placement at the level of the aortic root, and independent of catheter access site and patient position.

Ketorolac reduces postoperative narcotic requirements.

BACKGROUND/PURPOSE: Adverse effects from narcotics complicate pain management in children. Ketorolac, a potent nonsteroidal antiinflammatory agent can be used as an adjuvant analgesic, yet concerns of bleeding and nephrotoxicity have limited routine use. The authors hypothesized that postoperative use of ketorolac in healthy pediatric surgical patients would limit narcotic requirements without increasing morbidity. METHODS: A case-control clinical trial was conducted of 29 pediatric surgical cases prospectively administered ketorolac (0.5 mg/kg intravenously every 6 hours) supplemented with morphine. Controls receiving morphine only were matched for age (+/- 6 months) and surgical procedure. Incidence of respiratory depression, urinary retention, emesis, nephrotoxicity, and bleeding were recorded. RESULTS: Patients receiving ketorolac plus morphine had significantly less morphine requirements in the first 48 postoperative hours (Ketorolac plus Morphine: 0.36+/-0.16 mg/kg/d, Morphine only: 1.08+/-0.16 mg/kg/d [P<.05, analysis by paired t test]). This decrease was noted despite mode of analgesia (patient controlled or nurse administered). Adverse effects of morphine including respiratory depression, emesis, and urinary retention were not affected by ketorolac. Patients administered ketorolac had no significant increase in bleeding or nephrotoxicity. CONCLUSION: Ketorolac exhibits significant opiate-sparing effects in the immediate postoperative period without introducing additional morbidity to pediatric surgical procedures.

Matrix metalloproteinase inhibitor: differential effects on pulmonary neutrophil and monocyte sequestration following cardiopulmonary bypass.

UNLABELLED: Acute respiratory distress syndrome (ARDS) following cardiopulmonary bypass (CPB), also known as "post-pump" or "post-perfusion syndrome" (PPS), results from sequential priming and activation of neutrophils. We hypothesized that chemically modified tetracycline (CMT-3) an inhibitor of neutrophil matrix metalloproteinase (MMP) and elastase, would prevent PPS. We performed histometric analysis of lung tissue from our porcine PPS model to correlate cellular sequestration and histologic injury with CMT-3 treatment. METHODS: Yorkshire pigs were randomized into five groups: Control (n = 3); CPB (n = 5); femoral-femoral bypass 1 hour; LPS (n = 7), Escherichia coli lipopolysaccharide (1 microgram/kg); CPB + LPS (n = 6); and CPB + LPS + CMT (n = 5), sequential insults and CMT-3. Protocol histometric analysis defined cellular and tissue components of lung injury. RESULTS: CMT-3 decreased neutrophil sequestration in the CPB + LPS + CMT-3 group (p < 0.0001 vs. CPB + LPS). There were no differences in monocytes between CPB + LPS and CPB + LPS + CMT treatment groups. CONCLUSIONS: CMT-3 attenuates neutrophil sequestration but has no effect on mononuclear sequestration in our PPS model. This finding supports current research on leukocyte chemokines and has important implications regarding mechanisms of CMT-3. Despite lack of monocyte response to CMT-3, PPS was prevented by inhibiting neutrophils alone; confirming the primary role of neutrophils in PPS.

Alterations in t-butylbicyclophosphorothionate binding in the brains of lidocaine-kindled rats.

This autoradiographic study examines regional GABAA receptors in lidocaine-kindled rats. [35S]t-Butylbicyclophosphorothionate (TBPS), which binds in or near the chloride channel, was used to radiolabel GABAA complexes. Male Sprague-Dawley rats were injected daily with lidocaine (65mg/kg, i.p.). Seizure activity was evaluated using the Racine Scale (Racine, 1972). The animals displayed a gradual increase in the indices and by day 20 greater than 50% were in stage 4 or 5. Regression of behavior was seen in half of the experimental group and this subgroup was considered 'compensated'. Autoradiographs were analyzed using a computer-based image analysis system. Several regions within the kindled group display a decrease in TBPS binding, including the subiculum, posterior lateral thalamic nuclei, the lateral hippocampus CA1, and the lateral hippocampus CA3. Conversely, within the compensated group these regions display normal or heightened TBPS binding. The data support the theory that alterations in the GABAA receptors are involved in the kindling model of epilepsy.

Double blind evaluation of long acting diethylpropion hydrochloride in obese patients from a general practice.

Obese patients encountered in general practice were studied in order to determine whether a long-acting form of diethylpropion hydrochloride (Tenuate Dospan) was more effective than placebo for weight loss. One hundred and two patients completed this double blind, 16-week crossover study. During the first eight weeks, the patients treated with diethylpropion hydrochloride lost significantly (P smaller than 0.001) more weight than the patients treated with placebo (an average of 11-1 lb or 6-4% of their initial weight as compared with 6-2 lb or 3-6% of their initial weight). When the group taking diethylpropion hydrochloride crossed over to placebo for a second eight weeks, they lost an average of 1-5 lb (0-9% of their weight at the start of the second period), while the group who crossed from placebo over to diethylpropion hydrochloride lost an average of 6-7 lb (3-8%). The advantages of diethylpropion hydrochloride over placebo are statistically significant.

Risk factors for acute chest syndrome in children with sickle cell disease undergoing abdominal surgery.

BACKGROUND/PURPOSE: The reported incidence of acute chest syndrome (ACS) in children with sickle cell disease (SCD) is 15% to 20%. Our current objective was to assess risk factors and morbidity associated with ACS. METHODS: The authors reviewed the outcome of children with SCD undergoing abdominal surgery over a 10-year period. RESULTS: From 1991 to 2003, 60 children underwent laparoscopic cholecystectomy (LC; n = 29), laparoscopic splenectomy (LS; n = 28), or both (LB; n = 3). Mean age was 8.6 (0.7 to 20) years, and 35 (58%) were boys. Fifty-four (90%) had a preoperative hemoglobin greater than 10 g/dL, but only 22 (37%) received routine oxygen after surgery. No surgery was converted to an open procedure. Four children (6.6%), all of whom underwent either LS or LB, had ACS associated with an increased length of stay (7.4 +/- 2.4 days) but no mortality. Factors associated with the development of ACS were age (3.0 +/- 1.7 v 9.4 +/- 5.7 years; P =.03), weight (12.1 +/- 3.0 v 32.6 +/- 18.2 kg; P =.04), operative blood loss (3.2 +/- 0.5 v 1.4 +/- 1.2 mL/kg; P =.03), and final temperature in the operating room (OR; 36.2 +/- 0.4 v 37.6 +/- 0.4 degrees C; P =.01). ACS was not significantly related to duration of surgery, OR fluids, or oxygen usage. CONCLUSIONS: Younger children with greater blood and heat loss during surgery appear more prone to ACS. Splenectomy also seems to increase the risk of ACS. The authors' current incidence (6.6%) of ACS in children with SCD undergoing abdominal surgery is much lower than previously reported. This may be explained by the aggressive use of preoperative blood transfusion or more routine use of laparoscopy.

Visual validation of the mechanical stabilizing effects of positive end-expiratory pressure at the alveolar level.

BACKGROUND: Positive end-expiratory pressure (PEEP) reduces ventilator-induced lung injury (VILI), presumably by mechanically stabilizing alveoli and decreasing intrapulmonary shear. Although there is indirect support for this concept in the literature, direct evidence is lacking. In a surfactant depletion model of acute lung injury we observed unstable alveolar mechanics referred to as repeated alveolar collapse and expansion (RACE) as measured by changes in alveolar area from inspiration to expiration (I - E(Delta)). We tested the hypothesis that over a range of tidal volumes PEEP would prevent RACE by mechanically stabilizing alveoli. MATERIALS AND METHODS: Yorkshire pigs were randomized to three groups: control (n = 4), Tween (surfactant-deactivating detergent) (n = 4), and Tween + PEEP (7 cm H(2)O) (n = 4). Using in vivo video microscopy individual alveolar areas were measured with computer image analysis at end inspiration and expiration over consecutive increases in tidal volume (7, 10, 15, 20, and 30 cc/kg.) I - E(Delta) was calculated for each alveolus. RESULTS: Surfactant deactivation significantly increased I - E(Delta) at every tidal volume compared to controls (P < 0.05). PEEP prevented this change, returning I - E(Delta) to control levels over a spectrum of tidal volumes. CONCLUSIONS: RACE occurs in our surfactant deactivation model of acute lung injury. PEEP mechanically stabilizes alveoli and prevents RACE over a range of tidal volumes. This is the first study to visually document the existence of RACE and the mechanical stabilizing effects of PEEP at the alveolar level. The ability of PEEP to stabilize alveoli and reduce shear during mechanical ventilation has important implications for therapeutic strategies directed at VILI and acute respiratory distress syndrome.

Altered alveolar mechanics in the acutely injured lung.

OBJECTIVES: Alterations in alveolar mechanics (i.e., the dynamic change in alveolar size during tidal ventilation) are thought to play a critical role in acute lung injuries such as acute respiratory distress syndrome (ARDS). In this study, we describe and quantify the dynamic changes in alveolar mechanics of individual alveoli in a porcine ARDS model by direct visualization using in vivo microscopy. DESIGN: Prospective, observational, controlled study. SETTING: University research laboratory. SUBJECTS: Ten adult pigs. INTERVENTIONS: Pigs were anesthetized and placed on mechanical ventilation, underwent a left thoracotomy, and were separated into the following two groups post hoc: a control group of instrumented animals with no lung injury (n = 5), and a lung injury group in which lung injury was induced by tracheal Tween instillation, causing surfactant deactivation (n = 5). Pulmonary and systemic hemodynamics, blood gases, lung pressures, subpleural blood flow (laser Doppler), and alveolar mechanics (in vivo microscopy) were measured in both groups. Alveolar size was measured at peak inspiration (I) and end expiration (E) on individual subpleural alveoli by image analysis. Histologic sections of lung tissue were taken at necropsy from the injury group. MEASUREMENTS AND MAIN RESULTS: In the acutely injured lung, three distinct alveolar inflation-deflation patterns were observed and classified: type I alveoli (n = 37) changed size minimally (I - EDelta = 367 +/- 88 microm2) during tidal ventilation; type II alveoli (n = 37) changed size dramatically (I - EDelta = 9326 +/- 1010 microm2) with tidal ventilation but did not totally collapse at end expiration; and type III alveoli (n = 12) demonstrated an even greater size change than did type II alveoli (I - EDelta = 15,418 +/- 1995 microm2), and were distinguished from type II in that they totally collapsed at end expiration (atelectasis) and reinflated during inspiration. We have termed the abnormal alveolar inflation pattern of type II and III alveoli "repetitive alveolar collapse and expansion" (RACE). RACE describes all alveoli that visibly change volume with ventilation, regardless of whether these alveoli collapse totally (type III) at end expiration. Thus, the term "collapse" in RACE refers to a visibly obvious collapse of the alveolus during expiration, whether this collapse is total or partial. In the normal lung, all alveoli measured exhibited type I mechanics. Alveoli were significantly larger at peak inspiration in type II (18,266 +/- 1317 microm2, n = 37) and III (15,418 +/- 1995 microm2, n = 12) alveoli as compared with type I (8214 +/- 655 microm2, n = 37). Tween caused a heterogenous lung injury with areas of normal alveolar mechanics adjacent to areas of abnormal alveolar mechanics. Subsequent histologic sections from normal areas exhibited no pathology, whereas lung tissue from areas with RACE mechanics demonstrated alveolar collapse, atelectasis, and leukocyte infiltration. CONCLUSION: Alveolar mechanics are altered in the acutely injured lung as demonstrated by the development of alveolar instability (RACE) and the increase in alveolar size at peak inspiration. Alveolar instability varied from alveolus to alveolus in the same microscopic field and included alveoli that changed area greatly with tidal ventilation but remained patent at end expiration and those that totally collapsed and reexpanded with each breath. Thus, alterations in alveolar mechanics in the acutely injured lung are complex, and attempts to assess what may be occurring at the alveolar level from analysis of inflection points on the whole-lung pressure/volume curve are likely to be erroneous. We speculate that the mechanism of ventilator-induced lung injury may involve altered alveolar mechanics, specifically RACE and alveolar overdistension.

Cecal volvulus: a report of two cases occurring after the antegrade colonic enema procedure.

BACKGROUND: Many children with chronic constipation and fecal incontinence have benefited from the antegrade colonic enema (ACE) procedure. Routine antegrade colonic lavage often allows such children to avoid daytime soiling. This report describes 2 children in whom the ACE procedure was complicated by a cecal volvulus. METHODS: A retrospective review of 164 children with an ACE procedure was conducted. Two instances of cecal volvulus were identified. RESULTS: The first child presented with abdominal pain and difficulty intubating the ACE site. Over the subsequent day, his pain worsened, and radiographs depicted a colonic obstruction. At laparotomy, a cecal volvulus resulting in bowel necrosis was observed, and resection of the affected bowel and appendix (in the right lower quadrant) and end ileostomy was required. He subsequently had the stoma closed and a new ACE constructed with a colon flap. The second child presented with shock and evidence of an acute abdomen. At laparotomy, a cecal volvulus was noted, and ileocolic resection including the ACE stoma (located at the umbilicus) and an ileostomy and Hartmann pouch was performed. He had a protracted hospital course requiring ventilator and inotropic support. He currently is well and still has an ileostomy stoma. CONCLUSIONS: A high index of suspicion for a potentially life-threatening cecal volvulus should be maintained in children undergoing an ACE procedure who present with abdominal pain, evidence of bowel obstruction, or difficulty in advancing the ACE irrigation catheter.

Metalloproteinase inhibition prevents acute respiratory distress syndrome.

BACKGROUND: The acute respiratory distress syndrome (ARDS) occurs in patients with clearly identifiable risk factors, and its treatment remains merely supportive. We postulated that patients at risk for ARDS can be protected against lung injury by a prophylactic treatment strategy that targets neutrophil-derived proteases. We hypothesized that a chemically modified tetracycline 3 (COL-3), a potent inhibitor of neutrophil matrix metalloproteinases (MMPs) and neutrophil elastase (NE) with minimal toxicity, would prevent ARDS in our porcine endotoxin-induced ARDS model. METHODS: Yorkshire pigs were anesthetized, intubated, surgically instrumented for hemodynamic monitoring, and randomized into three groups: (1) control (n = 4), surgical instrumentation only; (2) lipopolysaccharide (LPS) (n = 4), infusion of Escherichia coli lipopolysaccharide at 100 microg/kg; and (3) COL-3 + LPS (n = 5), ingestion of COL-3 (100 mg/kg) 12 h before LPS infusion. All animals were monitored for 6 h following LPS or sham LPS infusion. Serial bronchoalveolar lavage (BAL) samples were analyzed for MMP concentration by gelatin zymography. Lung tissue was fixed for morphometric assessment at necropsy. RESULTS: LPS infusion was marked by significant (P < 0.05) physiological deterioration as compared with the control group, including increased plateau airway pressure (P(plat)) (control = 15.7 +/- 0.4 mm Hg, LPS = 23.0 +/- 1.5 mm Hg) and a decrement in arterial oxygen partial pressure (P(a)O(2)) (LPS = 66 +/- 15 mm Hg, Control = 263 +/- 25 mm Hg) 6 h following LPS or sham LPS infusion, respectively. Pretreatment with COL-3 reduced the above pathophysiological changes 6 h following LPS infusion (P(plat) = 18.5 +/- 1.7 mm Hg, P(a)O(2) = 199 +/- 35 mm Hg; P = NS vs control). MMP-9 and MMP-2 concentration in BAL fluid was significantly increased between 2 and 4 h post-LPS infusion; COL-3 reduced the increase in MMP-9 and MMP-2 concentration at all time periods. Morphometrically LPS caused a significant sequestration of neutrophils and monocytes into pulmonary tissue. Pretreatment with COL-3 ameliorated this response. The wet/dry lung weight ratio was significantly greater (P < 0.05) in the LPS group (10.1 +/- 1.0 ratio) than in either the control (6.4 +/- 0.5 ratio) or LPS+COL-3 (7.4 +/- 0.6 ratio) group. CONCLUSIONS: A single prophylactic treatment with COL-3 prevented lung injury in our model of endotoxin-induced ARDS. The proposed mechanism of COL-3 is a synergistic inhibition of the terminal neutrophil effectors MMPs and NE. Similar to the universal practice of prophylaxis against gastric stress ulceration and deep venous thromboses in trauma patients, chemically modified tetracyclines may likewise be administered to prevent acute lung injury in critically injured patients at risk of developing ARDS.

The mechanism of lung volume change during mechanical ventilation.

To understand ventilator-induced lung injury (VILI) during positive pressure ventilation, mechanisms of normal alveolar mechanics must first be established. Isotropic "balloonlike" alveolar volume (VA) change has been viewed as the prevailing mechanism of normal lung volume (VL) changes. We hypothesized that change in VL is predominantly caused by alveolar recruitment-derecruitment (R/D). Fifteen mongrel dogs were anesthetized and intubated with a tracheal divider. Through a thoracotomy incision, in vivo microscopy of subpleural alveoli was performed as the degassed lung was inflated to 80% TLC, and then deflated to residual volume (RV). Still photomicrographs were evaluated to determine if change in VL is due to change in VA or R/D of alveoli. We noted a steady, significant increase in alveolar recruitment as VL increased to 80% TLC (p < 0.05). However, VA increased significantly, but only to 20% TLC (p < 0.05). Once recruited, alveoli did not demonstrate any further volume change, whereas the lung as a whole maintained a normal pressure/volume relationship. In our model, changes in VL predominantly are caused by R/D.

Soluble tumor necrosis factor receptor prevents post-pump syndrome.

Post-pump syndrome is an acute lung injury following cardiopulmonary bypass (CPB) which is indistinguishable from the adult respiratory distress syndrome (ARDS). Tumor necrosis factor (TNF) is central to the inflammatory process and is capable of triggering the entire pathophysiologic response leading to ARDS. We hypothesized that treatment with a soluble TNF receptor-binding protein (TNFbp) would reduce the increase in serum TNF and prevent acute lung injury in our sequential insult model of ARDS following CPB. Anesthetized pigs were randomized to one of three groups: Control (n = 3), surgical preparation only; CPB + LPS (n = 6), femoral-femoral hypothermic bypass for 1 h followed by infusion of low dose Escherichia coli lipopolysaccharide (LPS; 1 microg/kg); and TNFbp + CPB + LPS (n = 4), pretreatment with intravenous TNFbp (2 mg/kg) followed immediately by both insults. CPB + LPS caused severe lung injury demonstrated by a significant fall in PaO2 and an increase in both intrapulmonary shunt and peak airway pressure as compared to all groups (P < 0.05). These changes were associated with a significant increase in plasma TNF level and pulmonary neutrophil sequestration. TNFbp significantly reduced plasma levels of TNF and prevented the lung injury typically observed with this ARDS model, but did not reduce pulmonary neutrophil sequestration. Thus, elevated serum TNF is not responsible for neutrophil sequestration but does play a role in neutrophil activation which causes lung injury. Prophylactic use of TNFbp in CPB patients may prevent neutrophil activation and reduce the incidence of post-pump ARDS.