Joseph DiRocco

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.

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.

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 cmH₂O 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.

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.

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.

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 (R ² = 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.

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 H2O, peak inflation pressure 14 cm H2O) or injurious ventilation (VILI group: respiratory rate 20 min–1, positive end-expiratory pressure 0 cm H2O, peak inflation pressure 45 cm H2O). Parameters studied included hemodynamics, pulmonary variables, in vivovideo 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.

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.