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.

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.

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.

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.