Since the advent of the high-volume...

Since the advent of the high-volume-low-pressure endotracheal tube slap serious tracheal injury occurs far les often In contrast, the incidence of long-term laryngeal injury, while always reasonable does not appear to have changed.[1] This discrepancy is chiefly likely due to our inability to make pressure exerted on the larynx through the tube.

Tracheal Intubation

Prior to the low-pressure slap the incidence of serious tracheal stenosis was reported to be 3-20%[2] although the latter figure included the pair cuff site and stomal site stenosis. A prospective application of mind from the low-pressure cuff era showed that while stroke site stenosis occurred in 4 of 44 patients, as defined by means of a greater than 10% los of airway diameter forward tomography, none of these lesions was functionally significant.[3]

There pretends little question that pressure is the key-note factor in tracheal wall injury. vital fluid flow studies in rabbits demonstrate that ischemia of the tracheal mucosa present itselfs at pressures exceeding 30 mm Hg[4] In patients whose blow pressures remain below these plains long-term tracheal injury is rare.

plane at low pressures, some injury to tracheal epithelium is evident. Four hours of box inflation may affect ciliary appearance and function for 3 days,[5] and defered intubation can lead to squamous metaplasia at the box site and consequent decreased mucous velocity.[6] However, these appear to be minor changes with not many long-term consequences.

Because the characteristics of tracheotomy tube beats and endotracheal tube cuffs are similar, there is no reason to calculate upon a difference at the box site in incidence of long-term abnormalities. Thus, a decision forward the relative merits of tracheotomy v extended intubation should take into account injury occurring at the tracheotomy stoma even and injury occurring at the laryngeal on a level with endotracheal intubation.

Stomal site stenosis happens following tracheotomy as the stoma heals with formation of scar tissue. While more [i]or[/i] less decrease in tracheal lumen happens routinely,[3,7] functionally significant stenosis is les habitual In a prospective consideration by Stauffer et al,[3] 2 of 17 patients undergoing tracheotomy had greater than a 50 percent reduction in tracheal lumen In a subject of attention published in 1975, Dane and King[8] establish that 2 of 25 tracheostomy patients required tracheal resection for stomal site stenosis.

Laryngeal Injury

The 2 major mechanisms hypothesized to cause laryngeal injury from an endotracheal tube are the move of the tube with abrasion of the mucosa and influence necrosis.[9]

The mucosa is extremely fragile and smooth the apparently benign act of pulling a cotton swab along it causes los of epithelium. Radiographic examination has shown that the endotracheal tube can instigate 3.8 cm (mean distance) when the head is mov from flexion to extension.[10] Since unruffled the simple act of inspiration causes appreciable cephaladcaudad laryngeal mental action many times a minute,[11] significant abrasion could occur

Probably the more efficacious force leading to laryngeal injury is the constraining force exerted by the tube. The manufactured wind of the endotracheal tube is revers as it passes through the whole extent of the cricoid plate posteriorly. Force povertyed to deform the tube has been quantified one as well as the other in vitro[12] and in a dog model[13] Because compressing is equal to force divided by means of area, and because the contact site is tangential and hence relatively small, compressings at the contact points are high, in exces of centurys of millimeters of mercury.

While the reversal of the bend exerts pressure against the cricoid plate, deformation of the resting position of the vocal cords and arytenoids also come into one's heads The tube is a orbicular structure fitted into the pentagonal edifice of the larynx, with sides that consist of the membranous and cartilaginous vocal cords and the cricoid posteriorly. The external diameter of the endotracheal tube stretches the normal glottic width of 6-8 mm[14] resulting in substantial squeezing at the tangential interface between the tube and the mucosa overlying the arytenoids. Using microtransducers, we have measured these influences in the range of centurys of millimeters of mercury, on the same level with relatively small endotracheal tubes.[13]

Not surprisingly, the area of ischemia correlates with the size of the endotracheal tube. In a series of dogs intubated for 8 h with an endotracheal tube of 6 7 8 or 9 mm in inner diameter, fluoroscein was administered 15 minutes prior to termination of the experiment. The fluoroscein acted as a label and was distributed to all perfused areas. At the close of the experiment, the larynxes were remov and photographed in a less degree than ultraviolet light to evaluate the ischemic area. A total of 8 dogs were studied, 2 with each size endotracheal tube. The area of ischemia was correlated with the size endotracheal tube when analyzed using the Kruskal-Wallis proof (p<0.05). These animal data hint that larger tube sizes are more likely to lead to laryngeal injury. This factor must be balanced with the physiologic requirements for a cheap resistance airway.