Pedunculated colonic lipoma prolapsing through the anus.

Colorectal lipomas are the second most common benign tumors of the colon. These masses are typically incidental findings with over 94% being asymptomatic. Symptoms-classically abdominal pain, bleeding per rectum and alterations in bowel habits-may arise when lipomas become larger than 2 cm in size. Colonic lipomas are most often noted incidentally by colonoscopy. They may also be identified by abdominal imaging such as computed tomography or magnetic resonance imaging. We report a case of a sixty-one years old male who presented to our emergency room with a 6.7 cm × 6.3 cm soft tissue mucosal mass protruding transanally. The patient was stable with a benign abdominal examination. The mass was initially thought to be a rectal prolapse; however, a limited digital rectal exam was able to identify this as distinct from the anal canal. Since the mass was irreducible, it was elected to be resected under anesthesia. At surgery, manipulation of the mass identified that the lesion was pedunculated with a long and thickened stalk. A laparoscopic linear cutting stapler was used to resect the mass at its stalk. Pathology showed a polypoid submucosal lipoma of the colon with overlying ulceration and necrosis. We report this case to highlight this rare but possible presentation of colonic lipomas; an incarcerated, trans-anal mass with features suggesting rectal prolapse. Trans-anal resection is simple and effective treatment.

Endoscopic fixation of the rectum for rectal prolapse: a feasibility and survival experimental study.

BACKGROUND: In recent years, there has been considerable interest in developing technology as well as techniques that could widen the therapeutic horizons of endoscopy. Rectal prolapse, a benign localized condition causing considerable morbidity, could be an excellent focus for new endoscopic therapies. The aim of this study was to assess the feasibility and safety of endoluminal fixation of the rectum to the anterior abdominal wall, after pushing it up inside the body, using an in vivo animal model. METHODS: We performed an in vivo comparative surgical study in a porcine model, including laparoscopic mobilization of the rectum and posterior rectopexy (standard surgical method) or endoluminal tacking of the rectum. After proving feasibility in ex vivo and acute studies, we performed a survival study to evaluate the safety of endoluminal tacking of the mobilized rectum to the anterior abdominal wall. The main outcome measures were successful completion of the tasks, maintenance of the fixation, complications associated with the methods, and survival studies including histopathological examinations of the fixation sites. RESULTS: There were two groups: laparoscopic rectopexy (8 animals) and endoluminal fixation of the rectum to the anterior abdominal wall (10 animals). There were no differences between these two groups in their postoperative recovery. The group with the endoluminal fixation was found to have adequate attachment of the rectum to the anterior abdominal wall (measured attachment pressure in the endoluminal group = 6.06 ± 0.52 ft-lb, in the control group = 4.86 ± 2.00 ft-lb) on both gross and microscopic evaluation. CONCLUSION: Endoscopic fixation of the mobilized rectum is feasible and safe in this model and in the future may provide an effective alternative to current treatment options for rectal prolapse.

Comparison of "open lung" modes with low tidal volumes in a porcine lung injury model.

BACKGROUND: Ventilator strategies that maintain an "open lung" have shown promise in treating hypoxemic patients. We compared three "open lung" strategies with standard of care low tidal volume ventilation and hypothesized that each would diminish physiologic and histopathologic evidence of ventilator induced lung injury (VILI). MATERIALS AND METHODS: Acute lung injury (ALI) was induced in 22 pigs via 5% Tween and 30-min of injurious ventilation. Animals were separated into four groups: (1) low tidal volume ventilation (LowVt -6 mL/kg); (2) high-frequency oscillatory ventilation (HFOV); (3) airway pressure release ventilation (APRV); or (4) recruitment and decremental positive-end expiratory pressure (PEEP) titration (RM+OP) and followed for 6 h. Lung and hemodynamic function was assessed on the half-hour. Bronchoalveolar lavage fluid (BALF) was analyzed for cytokines. Lung tissue was harvested for histologic analysis. RESULTS: APRV and HFOV increased PaO(2)/FiO(2) ratio and improved ventilation. APRV reduced BALF TNF-α and IL-8. HFOV caused an increase in airway hemorrhage. RM+OP decreased SvO(2), increased PaCO(2), with increased inflammation of lung tissue. CONCLUSION: None of the "open lung" techniques were definitively superior to LowVt with respect to VILI; however, APRV oxygenated and ventilated more effectively and reduced cytokine concentration compared with LowVt with nearly indistinguishable histopathology. These data suggest that APRV may be of potential benefit to critically ill patients but other "open lung" strategies may exacerbate injury.

The role of time and pressure on alveolar recruitment.

Inappropriate mechanical ventilation in patients with acute respiratory distress syndrome can lead to ventilator-induced lung injury (VILI) and increase the morbidity and mortality. Reopening collapsed lung units may significantly reduce VILI, but the mechanisms governing lung recruitment are unclear. We thus investigated the dynamics of lung recruitment at the alveolar level. Rats (n = 6) were anesthetized and mechanically ventilated. The lungs were then lavaged with saline to simulate acute respiratory distress syndrome (ARDS). A left thoracotomy was performed, and an in vivo microscope was placed on the lung surface. The lung was recruited to three recruitment pressures (RP) of 20, 30, or 40 cmH(2)O for 40 s while subpleural alveoli were continuously filmed. Following measurement of microscopic alveolar recruitment, the lungs were excised, and macroscopic gross lung recruitment was digitally filmed. Recruitment was quantified by computer image analysis, and data were interpreted using a mathematical model. The majority of alveolar recruitment (78.3 +/- 7.4 and 84.6 +/- 5.1%) occurred in the first 2 s (T2) following application of RP 30 and 40, respectively. Only 51.9 +/- 5.4% of the microscopic field was recruited by T2 with RP 20. There was limited recruitment from T2 to T40 at all RPs. The majority of gross lung recruitment also occurred by T2 with gradual recruitment to T40. The data were accurately predicted by a mathematical model incorporating the effects of both pressure and time. Alveolar recruitment is determined by the magnitude of recruiting pressure and length of time pressure is applied, a concept supported by our mathematical model. Such a temporal dependence of alveolar recruitment needs to be considered when recruitment maneuvers for clinical application are designed.

Alveolar instability caused by mechanical ventilation initially damages the nondependent normal lung.

BACKGROUND: Septic shock is often associated with acute respiratory distress syndrome, a serious clinical problem exacerbated by improper mechanical ventilation. Ventilator-induced lung injury (VILI) can exacerbate the lung injury caused by acute respiratory distress syndrome, significantly increasing the morbidity and mortality. In this study, we asked the following questions: what is the effect of the lung position (dependent lung versus nondependent lung) on the rate at which VILI occurs in the normal lung? Will positive end-expiratory pressure (PEEP) slow the progression of lung injury in either the dependent lung or the nondependent lung? MATERIALS AND METHODS: Sprague-Dawley rats (n = 19) were placed on mechanical ventilation, and the subpleural alveolar mechanics were measured with an in vivo microscope. Animals were placed in the lateral decubitus position, left lung up to measure nondependent alveolar mechanics and left lung down to film dependent alveolar mechanics. Animals were ventilated with a high peak inspiratory pressure of 45 cmH2O and either a low PEEP of 3 cmH2O or a high PEEP of 10 cmH2O for 90 minutes. Animals were separated into four groups based on the lung position and the amount of PEEP: Group I, dependent + low PEEP (n = 5); Group II, nondependent + low PEEP (n = 4); Group III, dependent + high PEEP (n = 5); and Group IV, nondependent + high PEEP (n = 5). Hemodynamic and lung function parameters were recorded concomitant with the filming of alveolar mechanics. Histological assessment was performed at necropsy to determine the presence of lung edema. RESULTS: VILI occurred earliest (60 min) in Group II. Alveolar instability eventually developed in Groups I and II at 75 minutes. Alveoli in both the high PEEP groups were stable for the entire experiment. There were no significant differences in arterial PO2 or in the degree of edema measured histologically among experimental groups. CONCLUSION: This open-chest animal model demonstrates that the position of the normal lung (dependent or nondependent) plays a role on the rate of VILI.

Using pressure-volume curves to set proper PEEP in acute lung injury.

The evolution of respiratory care on patients with acute respiratory distress syndrome (ARDS) has been focused on preventing the deleterious effects of mechanical ventilation, termed ventilator-induced lung injury (VILI). Currently, reduced tidal volume is the standard of ventilatory care for patients with ARDS. The current focus, however, has shifted to the proper setting of positive end-expiratory pressure (PEEP). The whole lung pressure-volume (P/V) curve has been used to individualize setting proper PEEP in patients with ARDS, although the physiologic interpretation of the curve remains under debate. The purpose of this review is to present the pros and cons of using P/V curves to set PEEP in patients with ARDS. A systematic analysis of recent and relevant literature was conducted. It has been hypothesized that proper PEEP can be determined by identifying P/V curve inflection points. Acquiring a dynamic curve presents the key to the curve's bedside application. The lower inflection point of the inflation limb has been shown to be the point of massive alveolar recruitment and therefore an option for setting PEEP. However, it is becoming widely accepted that the upper inflection point (UIP) of the deflation limb of the P/V curve represents the point of optimal PEEP. New methods used to identify optimal PEEP, including tomography and active compliance measurements, are currently being investigated. In conclusion, we believe that the most promising method for determining proper PEEP settings is use of the UIP of the deflation limb. However, tomography and dynamic compliance may offer superior bedside availability.

A 4-dimensional model of the alveolar structure.

The alveolar structure, a space-filling branching duct system with alveolar openings, is one of the most complicated structures in the living body. Although its deformation during ventilation is the basic knowledge for lung physiology, there has been no consensus on it because of technical difficulties of dynamic 3-dimensional observation in vivo. It is known that the alveolar duct wall (primary septa) in the fetal lung is deformed so as to obtain the largest inner space and the widest surface area, and that the secondary septa grow just before birth and their free ridges form the alveolar entrance rings (mouths) containing abundant elastin fibers. We have constructed a 4-dimensional alveolar model according to this morphogenetic process, where the alveolar deformation is modeled by a combination of springs and hinges, corresponding to elastin fibers at alveolar mouths and junctions of alveolar septa, respectively. The model includes a hypothesis that alveolar mouths are closed at minimum volume and that closed alveoli are stabilized by the alveolar lining liquid film containing a surfactant. Morphometric characteristics of the model were consistent with previous reports. Furthermore, the model explained how the alveolar number and size could change during ventilation. Using in vivo microscopy, we validated our model by an analysis of the dynamic inflation and deflation of subpleural alveoli. Our model, including the alveolar mouth-closure hypothesis, can explain the origin of phase IV in a single breath nitrogen washout curve (closing volume) and mechanism of alveolar recruitment/derecruitment.

Correlation between alveolar recruitment/derecruitment and inflection points on the pressure-volume curve.

OBJECTIVE: To determine whether individual alveolar recruitment/derecruitment (R/D) is correlated with the lower and upper inflections points on the inflation and deflation limb of the whole-lung pressure-volume (P-V) curve. DESIGN AND SETTING: Prospective experimental study in an animal research laboratory. SUBJECTS: Five anesthetized rats subjected to saline-lavage lung injury. INTERVENTIONS: Subpleural alveoli were filmed continuously using an in vivo microscope during the generation of a whole-lung P-V curve using the super syringe technique. Alveolar R/D was correlated to the calculated inflection points on both limbs of the P-V curve. MEASUREMENTS AND RESULTS: There was continual alveolar recruitment along the entire inflation limb in all animals. There was some correlation (R2=0.898) between the pressure below which microscopic derecruitment was observed and the upper inflection point on the deflation limb. No correlation was observed between this pressure and the lower inflection point on the inflation limb. CONCLUSIONS: In this physiological experiment in lungs with pure surfactant deactivation we found that individual alveolar recruitment measured by direct visualization was not correlated with the lower inflection point on inflation whereas alveolar derecruitment was correlated with alveolar derecruitment on deflation. These data suggest that inflection points on the P-V curve do not always represent a change in alveolar number.

Absence of alveolar tears in rat lungs with significant alveolar instability.

BACKGROUND: Lung injury associated with the acute respiratory distress syndrome can be exacerbated by improper mechanical ventilation creating a secondary injury known as ventilator-induced lung injury (VILI). We hypothesized that VILI could be caused in part by alveolar recruitment/derecruitment resulting in gross tearing of the alveolus. OBJECTIVES: The exact mechanism of VILI has yet to be elucidated though multiple hypotheses have been proposed. In this study we tested the hypothesis that gross alveolar tearing plays a key role in the pathogenesis of VILI. METHODS: Anesthetized rats were ventilated and instrumented for hemodynamic and blood gas measurements. Following baseline readings, rats were exposed to 90 min of either normal ventilation (control group: respiratory rate 35 min(-1), positive end-expiratory pressure 3 cm H(2)O, peak inflation pressure 14 cm H(2)O) or injurious ventilation (VILI group: respiratory rate 20 min(-1), positive end-expiratory pressure 0 cm H(2)O, peak inflation pressure 45 cm H(2)O). Parameters studied included hemodynamics, pulmonary variables, in vivo video microscopy of alveolar mechanics (i.e. dynamic alveolar recruitment/derecruitment) and scanning electron microscopy to detect gross tears on the alveolar surface. RESULTS: Injurious ventilation significantly increased alveolar instability after 45 min and alveoli remained unstable until the end of the study (electron microscopy after 90 min revealed that injurious ventilation did not cause gross tears in the alveolar surface). CONCLUSIONS: We demonstrated that alveolar instability induced by injurous ventilation does not cause gross alveolar tears, suggesting that the tissue injury in this animal VILI model is due to a mechanism other than gross rupture of the alveolus.

Effect of positive end-expiratory pressure and tidal volume on lung injury induced by alveolar instability.

INTRODUCTION: One potential mechanism of ventilator-induced lung injury (VILI) is due to shear stresses associated with alveolar instability (recruitment/derecruitment). It has been postulated that the optimal combination of tidal volume (Vt) and positive end-expiratory pressure (PEEP) stabilizes alveoli, thus diminishing recruitment/derecruitment and reducing VILI. In this study we directly visualized the effect of Vt and PEEP on alveolar mechanics and correlated alveolar stability with lung injury. METHODS: In vivo microscopy was utilized in a surfactant deactivation porcine ARDS model to observe the effects of Vt and PEEP on alveolar mechanics. In phase I (n = 3), nine combinations of Vt and PEEP were evaluated to determine which combination resulted in the most and least alveolar instability. In phase II (n = 6), data from phase I were utilized to separate animals into two groups based on the combination of Vt and PEEP that caused the most alveolar stability (high Vt [15 cc/kg] plus low PEEP [5 cmH2O]) and least alveolar stability (low Vt [6 cc/kg] and plus PEEP [20 cmH2O]). The animals were ventilated for three hours following lung injury, with in vivo alveolar stability measured and VILI assessed by lung function, blood gases, morphometrically, and by changes in inflammatory mediators. RESULTS: High Vt/low PEEP resulted in the most alveolar instability and lung injury, as indicated by lung function and morphometric analysis of lung tissue. Low Vt/high PEEP stabilized alveoli, improved oxygenation, and reduced lung injury. There were no significant differences between groups in plasma or bronchoalveolar lavage cytokines or proteases. CONCLUSION: A ventilatory strategy employing high Vt and low PEEP causes alveolar instability, and to our knowledge this is the first study to confirm this finding by direct visualization. These studies demonstrate that low Vt and high PEEP work synergistically to stabilize alveoli, although increased PEEP is more effective at stabilizing alveoli than reduced Vt. In this animal model of ARDS, alveolar instability results in lung injury (VILI) with minimal changes in plasma and bronchoalveolar lavage cytokines and proteases. This suggests that the mechanism of lung injury in the high Vt/low PEEP group was mechanical, not inflammatory in nature.

Chemically modified tetracycline (COL-3) improves survival if given 12 but not 24 hours after cecal ligation and puncture.

Sepsis can result in excessive and maladaptive inflammation that is responsible for more than 215,00 deaths per year in the United State alone. Current strategies for reducing the morbidity and mortality associated with sepsis rely on treatment of the syndrome rather than prophylaxis. We have been investigating a modified tetracycline, COL-3, which can be given prophylactically to patients at high risk for developing sepsis. Our group has shown that COL-3 is very effect at preventing the sequelae of sepsis if given before or immediately after injury in both rat and porcine sepsis models. In this study, we wanted to determine the "treatment window" for COL-3 after injury at which it remains protective. Sepsis was induced by cecal ligation and puncture (CLP). Rats were anesthetized and placed into five groups: CLP (n = 20) = CLP without COL-3, sham (n = 5) = surgery without CLP or COL-3, COL3@6h (n = 10) = COL-3 given by gavage 6 h after CLP, COL3@12h (n = 10) = COL-3 given by gavage 12 h after CLP, and COL3@24h (n = 20) = COL-3 given by gavage 24 h after CLP. COL-3 that was given at 6 and 12 h after CLP significantly improved survival as compared with the CLP and the CLP@24h groups. Improved survival was associated with a significant improvement in lung pathology assessed morphologically. These data suggest that COL-3 can be given up to 12 h after trauma and remain effective.

Isolated jejunal perforation after blunt thoracoabdominal trauma.

A case report of isolated jejunal perforation secondary to a relatively unique mechanism of blunt thoracoabdominal trauma is presented. A thorough and concise review of the multimodal approach that may be necessary to diagnose such a rare clinical problem is discussed.

Dynamic alveolar mechanics in four models of lung injury.

OBJECTIVE: To determine whether pathological alterations in alveolar mechanics (i.e., the dynamic change in alveolar size and shape with ventilation) at a similar level of lung injury vary depending on the cause of injury. DESIGN AND SETTING: Prospective controlled animal study in a university laboratory. SUBJECTS: 30 male Sprague-Dawley rats (300-550 g). INTERVENTIONS: Rats were separated into one of four lung injury models or control (n=6): (a) 2% Tween-20 (Tween, n=6), (b) oleic acid (OA, n=6), (c) ventilator-induced lung injury (VILI, PIP 40/ZEEP, n=6), (d) endotoxin (LPS, n=6). Alveolar mechanics were assessed at baseline and after injury (PaO2/FIO2 <300 mmHg) by in vivo microscopy. MEASUREMENTS: Alveolar instability (proportional change in alveolar size during ventilation) was used as a measurement of alveolar mechanics. RESULTS: Alveoli were unstable in Tween, OA, and VILI as hypoxemia developed (baseline vs. injury: Tween, 7+/-2% vs. 67+/-5%; OA: 3+/-2% vs. 82+/-9%; VILI, 4+/-2% vs. 72+/-5%). Hypoxemia after LPS was not associated with significant alveolar instability (baseline vs. injury: LPS, 3+/-2 vs. 8+/-5%). CONCLUSIONS: These data demonstrate that multiple pathological changes occur in dynamic alveolar mechanics. The nature of these changes depends upon the mechanism of lung injury.

Evidence of systemic cytokine release in patients undergoing cardiopulmonary bypass.

Cardiopulmonary bypass (CPB) causes a systemic inflammatory response syndrome (SIRS), which can progress to an acute lung inflammation known as postperfusion syndrome. We developed a two-phase hypothesis: first, that SIRS, as indicated by elevated cytokines post-CPB, would be correlated with postoperative pulmonary dysfunction (Phase I), and second, that the cytokine interleukin-6 (IL-6) is predominantly released from the heart in CPB patients (Phase II). Blood samples were collected from patients undergoing CPB for elective cardiac surgery. In seven patients (Phase I), arterial samples were drawn before, during (5 minutes and 60 minutes), and after CPB. In 14 patients (Phase II), samples were collected from the coronary sinus, superior vena cava, and a systemic artery at the times indicated previously. Samples were analyzed with enzyme-linked immunosorbent assay: IL-1, IL-6, IL-8, IL-10, and tumor necrosis factor-alpha were assessed in Phase I and IL-6 assessed in Phase II. In Phase I, IL-6, IL-8, and IL-10 were elevated after CPB, but only IL-6 concentrations correlated with lung function. In summary, Phase I data demonstrate that increased IL-6 levels at the end of CPB correlate with reduced lung function postoperatively. In Phase II, IL-6 elevation was similar at all sample sites suggesting that the heart is not the major source of IL-6 production. We suggest that IL-6 be implemented as a prognostic measure in patient care, and that patients with elevated IL-6 after CPB be targeted for more aggressive anti-inflammatory therapy to protect lung function.

Wood smoke inhalation causes alveolar instability in a dose-dependent fashion.

BACKGROUND: Wood smoke inhalation causes severe ventilation and oxygenation abnormalities. We hypothesized that smoke inhalation would cause lung injury by 2 mechanisms: (1) direct tissue injury by the toxic chemicals in the smoke and (2) a mechanical shear-stress injury caused by alveolar instability (ie, alveolar recruitment/derecruitment). We further postulated that alveolar instability would increase with the size of the cumulative smoke dose. METHODS: Anesthetized pigs were ventilated and instrumented for hemodynamic and blood-gas measurements. After baseline readings, the pigs were exposed to 5 separate doses of wood smoke, each dose lasting 1 min. Factors studied included hemodynamics, pulmonary variables, and in vivo photomicroscopy of alveolar mechanics (ie, the dynamic change in alveolar size with ventilation). RESULTS: Smoke inhalation significantly increased alveolar instability with 4 min and 5 min of smoke exposure. Significant rises in carboxyhemoglobin levels and in pulmonary shunt were also observed at 4 min and 5 min of smoke exposure. Lung histology demonstrated severe damage characteristic of acute lung injury. CONCLUSIONS: We demonstrated that wood smoke inhalation causes alveolar instability and that instability increases with each dose of smoke. These data suggest that smoke inhalation may cause a "2-hit" insult: the "first hit" being a direct toxic injury and the "second hit" being a shear-stress injury secondary to alveolar instability.

Pulmonary impedance and alveolar instability during injurious ventilation in rats.

The mechanical derangements in the acutely injured lung have long been ascribed, in large part, to altered mechanical function at the alveolar level. This has not been directly demonstrated, however, so we investigated the issue in a rat model of overinflation injury. After thoracotomy, rats were mechanically ventilated with either 1) high tidal volume (Vt) or 2) low Vt with periodic deep inflations (DIs). Forced oscillations were used to measure pulmonary impedance every minute, from which elastance (H) and hysteresivity (eta) were derived. Subpleural alveoli were imaged every 15 min using in vivo video microscopy. Cross-sectional areas of individual alveoli were measured at peak inspiration and end exhalation, and the percent change was used as an index of alveolar instability (%I-EDelta). Low Vt never led to an increase in %I-EDelta but did result in progressive atelectasis that coincided with an increase in H but not eta. DI reversed atelectasis due to low Vt, returning H to baseline. %I-EDelta, H, and eta all began to rise by 30 min of high Vt and were not reduced by DI. We conclude that simultaneous increases in both H and eta are reflective of lung injury in the form of alveolar instability, whereas an isolated and reversible increase in H during low Vt reflects merely derecruitment of alveoli.

Dynamic alveolar mechanics and ventilator-induced lung injury.

OBJECTIVES: To review the mechanism of dynamic alveolar mechanics (i.e., the dynamic change in alveolar size and shape during ventilation) in both the normal and acutely injured lung; to investigate the alteration in alveolar mechanics secondary to acute lung injury as a mechanism of ventilator-induced lung injury (VILI); and to examine the hypothesis that the reduced morbidity and mortality associated with protective strategies of mechanical ventilation is related to the normalization of alveolar mechanics. DATA EXTRACTION AND SYNTHESIS: This review is based on original published articles and review papers dealing with the mechanism of lung volume change at the alveolar level and the role of altered alveolar mechanics as a mechanism of VILI. In addition, data from our laboratory directly visualizing dynamic alveolar mechanics is reviewed and related to the literature. CONCLUSIONS: The mechanism of alveolar inflation in normal lungs is unclear. Nonetheless, normal alveoli are very stable and change size very little with ventilation. Acute lung injury causes marked destabilization of individual alveoli. Alveolar instability causes pulmonary damage and is believed to be a major component in the mechanism of VILI. Ventilator strategies that reduce alveolar instability may potentially reduce the morbidity and mortality associated with VILI.