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Objective The short-term safety of percutaneous dilatational tracheostomy has been widely demonstrated. However, less is known about their long-term complications. Through an illustrative case series, we present and define "corkscrew stenosis," a type of tracheal stenosis uniquely associated with percutaneous dilatational tracheostomy. Methods Patients treated at our institution for tracheal stenosis after percutaneous dilatational tracheostomy were reviewed. Demographic data including gender, age, history of presentation, lesion morphology, imaging, and management was collected and evaluated. The pathology of the stenosis and the strategies for prevention are presented. Results From January, 2008 through December 2011, 11 patients had tracheal stenosis after percutaneous dilatational tracheostomy. The mean age was 54 ± 17 years and 55% were male. The stenotic lesions were characterized by a corkscrew morphology at the stoma site with a mean distance of 2.3 ± 0.8 cm from the vocal cords. Images of these lesions demonstrated disruption and fracture of the proximal tracheal cartilages and displacement of the anterior tracheal wall into the tracheal lumen. The majority of our patients required tracheal resection for definitive repair. Conclusions We suggest that a unique form of tracheal stenosis can result from percutaneous dilatational tracheostomy. We observed corkscrew stenosis to be located proximally, associated with fractured tracheal rings, and morphologically appearing as interdigitation of these fractured rings. Recognizing corkscrew stenosis, its unique mechanism of formation, and technical means of prevention may be important in advancing the long-term safety of this procedure for critically ill patients who require prolonged ventilatory support.

The primary objective was to test the hypothesis that clinical re-expansion pulmonary edema is predominantly due to increased permeability of the alveolar-capillary barrier. A secondary objective was to determine if the alveolar epithelium was functionally intact in patients with re-expansion pulmonary edema by measuring net alveolar epithelial fluid transport in a subset of patients.Retrospective study of mechanically ventilated patients with re-expansion pulmonary edema.Two academic tertiary care hospitals.Seven patients with acute onset of re-expansion pulmonary edema after tube thoracostomy or thoracentesis.Pulmonary edema fluid and plasma were collected at the time of onset of re-expansion edema.Contrary to our hypothesis, the mean initial edema fluid to plasma protein ratio was 0.58+/-0.21, supporting a hydrostatic mechanism of edema formation. Four of the patients had an initial edema fluid to plasma protein ratio of less than 0.65, consistent with pure hydrostatic pulmonary edema, while the others had a slight increase in permeability (edema fluid to plasma ratios of 0.67, 0.71 and 0.77), perhaps due to capillary stress failure from hydrostatic stress. Alveolar fluid clearance (mean 9.8+/-8.0%/h) was intact in the subset of three patients in whom it was measured.This study provides the first direct evidence that hydrostatic forces may contribute to the development of re-expansion pulmonary edema.

In summary, long-term complications of artificial airways are rare but important sequelae of artificial airways. Many of the potential long-term complications of translaryngeal intubation and tracheotomy are similar and overlapping. Although most patients who undergo these procedures tend to tolerate them without difficulties, significant morbidity and mortality may occur. Identifying the exact cause of the complication may not be possible at times, due to the multiple risk factors involved in the pathogenesis. It is hoped that understanding these potential complications will lead to a more vigilant preventive measures during the institution of long-term artificial airways and a judicious early search for the underlying pathology when a complication is suspected.