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Respiration And The Airway:
M. Weiss, C. Doell, N. Koepfer, C. Madjdpour, K. Woitzek, and V. Bernet
Rapid pressure compensation by automated cuff pressure controllers worsens sealing in tracheal tubes
Br. J. Anaesth. 2009; 102: 273-278 [Abstract] [Full text] [PDF]
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Electronic letters published:

[Read E-letter] Continuous control of endotracheal cuff pressure
Saad Nseir   (12 March 2009)
[Read E-letter] Reply to "Histological Tracheal Surface Alterations by Hyperpressured Tracheal Tube Cuffs"
Markus Weiss, Markus Weiss   (5 February 2009)
[Read E-letter] Histological Tracheal Surface Alterations by Hyperpressured Tracheal Tube Cuffs
John George George Cherian   (2 February 2009)

Continuous control of endotracheal cuff pressure 12 March 2009
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Saad Nseir
Intensive Care Unit, Calmette Hosp, CHRU de Lille, FR

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Re: Continuous control of endotracheal cuff pressure

Editors, I read with interest the article by Dr. Weiss and colleagues [1]. The authors are to be congratulated for conducting such an interesting study with important implications in ICU patients. However, some clarifications regarding hyperinflation of cuff pressure, and sealing in tracheal tubes of ICU patients could be helpful. The authors stated that the implication of their findings is that in automated cuff pressure controllers, the cuff pressure set should be similar to peak inspiratory pressure to avoid cyclic up-and down regulation by these devices. In their in vitro study, pressure controlled ventilation was used with peak inspiratory pressure of 20, and 25 cmH2O. However, this ventilatory mode is rarely used in ICU patients, and most patients receive assist-control ventilation. In patients receiving assist- ventilation for acute lung injury, peak inspiratory pressure is frequently > 30 cmH2O. In addition, ischemic tracheal lesions result from hyperinflation (> 30 cmH2O) of endotracheal cuff. An endoscopic study performed in 40 patients undergoing surgery showed that obstruction of mucosal blood flow occurred at a lateral wall pressure above 30 cmH2O [2]. Further, in a study performed in intubated rabbits, superficial tracheal damage occurred within 15 minutes at lateral wall pressure of 27 cmH2O [3]. There was partial denuding of the basement membrane with a lateral wall pressure of 68 cmH2O. At a lateral wall pressure of 136 cmH2O, damage extended to the basement membrane and mucosal stroma within 15 minutes – and this damage was progressive with time. Therefore, overinflation of endotracheal cuff (> 30 cmH2O) should be avoided in intubated critically ill patients in order to prevent ischemic tracheal lesions. Variations in endotracheal cuff pressure are common in intubated critically ill patients. According to the results of a recent observationl cohort study performed in 101 ICU patients [4], only 18% of patients spent 100% of recording time with normal (20–30 cmH2O) cuff pressure. In addition, 33% of study patients developed underinflation or overinflation for more than 30 min. No modifiable risk factor for overinflation, and underinflation of cuff pressure could be identified in that study. These data suggest that continuous control of cuff pressure could be beneficial in ICU patient to prevent microaspiration and ischemic tracheal lesions. However, the study by Dr. Weiss and colleagues demonstrated that continuous control of endotracheal cuff pressure would be insufficient to prevent microaspiration and subsequent ventilator-associated pneumonia [1]. In fact, the automated cuff pressure controllers with rapid pressure correction (VBM Cuff Controller; Cuff Pressure Control TracoeTM ) interfered with the self-sealing mechanism of high sealing HVLP tube cuffs and reduceed their improved sealing characteristics. Recently, a pneumatic device was reported to provide effective continuous control of endotracheal cuff pressure in ventilated piglets [5], and mechanically ventilated ICU patients [6]. The Nosten® device (Leved, St- Maur, France) is a mechanical appliance that does not require a power supply. A sterile single-use 200 ml cylindrical cuff encased in a rigid compartment is connected to the endotracheal cuff with plastic tubing. A weight mounted on an articulated arm constantly exerts pressure on this cuff. This pressure can be adjusted by moving another weight along the arm to modulate the corresponding force, allowing the user to obtain the desired cuff pressure. Any variation is immediately cancelled out by the disproportion between the volumes of the two cuffs. Using such a device to continuously control cuff pressure would be helpful to avoid the interference observed with other devices by Dr. Weiss and colleagues, since variations in cuff pressure are smoothly and continuously corrected by the pneumatic device without any peak or drop in cuff pressure. However, further studies are required to confirm this hypothesis. The efficiency of this pneumatic device in controlling cuff pressure and reducing ischemic tracheal lesions was recently studied in ventilated piglets [5]. Twelve piglets were intubated and mechanically ventilated for 48 hours. Animals were randomized to manual control of the endotracheal cuff pressure (n = 6) or to continuous control of the endotracheal cuff pressure using a pneumatic device (n = 6). In the two groups, the endotracheal cuff was inflated with 50 ml air for 30 minutes, eight times daily in order to mimic high-pressure periods observed in intubated critically ill patients. In all animals, the cuff pressure and the airway pressure were continuously recorded for 48 hours. Whilst the pneumatic device provided effective continuous control of endotracheal cuff pressure, no significant difference was found in tracheal mucosal lesions of animals with or without a pneumatic device. Histologic examination demonstrated similar lesions in the two groups including, deep mucous ulceration, squamous metaplasic and interne mucosal inflammation.

Reference List

1. Weiss M, Doell C, Koepfer N, Madjdpour C, Woitzek K, and Bernet V: Rapid pressure compensation by automated cuff pressure controllers worsens sealing in tracheal tubes. Br J Anaesth 2009, 102:273-278.

2. Seegobin RD and van Hasselt GL: Endotracheal cuff pressure and tracheal mucosal blood flow: endoscopic study of effects of four large volume cuffs. Br Med J (Clin Res Ed) 1984, 288:965-968.

3. Nordin U: The trachea and cuff-induced tracheal injury. An experimental study on causative factors and prevention. Acta Otolaryngol Suppl 1977, 345:1-71.

4. Nseir S, Brisson H, Marquette CH, Chaud P, Di Pompeo C, Diarra M, and Durocher A: Variations in endotracheal cuff pressure in intubated critically ill patients: prevalence and risk factors. Eur J Anaesthesiol 2009, 26:229-234.

5. Nseir S, Duguet A, Copin MC, De jonckheere J, Zhang M, Similowski T, and Marquette CH: Continuous control of endotracheal cuff pressure and tracheal wall damage: a randomized controlled animal study. Crit Care 2007, 11:R109-

6. Duguet A, D'Amico L, Biondi G, Prodanovic H, Gonzalez-Bermejo J, and Similowski T: Control of tracheal cuff pressure: a pilot study using a pneumatic device. Intensive Care Med 2007, 33:128-132.

Conflict of Interest:

None declared

Reply to "Histological Tracheal Surface Alterations by Hyperpressured Tracheal Tube Cuffs" 5 February 2009
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Markus Weiss ,
Markus Weiss

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Re: Reply to "Histological Tracheal Surface Alterations by Hyperpressured Tracheal Tube Cuffs"

Sir,

I absolutely agree with Dr. John George George Cherian. It is of important scientific interest to find out if cyclic cuff pressure(self inflation at just seal pressure) or constant cuff pressure (e.g. 25 cm H2O) is more damaging to the tracheal mucosa. Histological investigations of tracheal surface are needed to obtain more evidence in this important issue.

Conflict of Interest:

None declared

Histological Tracheal Surface Alterations by Hyperpressured Tracheal Tube Cuffs 2 February 2009
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John George George Cherian
Fellow - Malaysian Institute of Medical Laboratory Sciences

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Re: Histological Tracheal Surface Alterations by Hyperpressured Tracheal Tube Cuffs

Sirs,

I read with interest Weiss et al's investigation on the integrity of sealing outcomes from employing automated cuff controllers as adjuncts during positive pressure ventilation and their efforts merit commendation.

It would be of sigificance if tracheal surface alterations secondary to cuff hyperpressure during cyclical variation of respiratory pressure could be ascertained histologically. Then, cuff pressure limits to avoid pathological tracheal surface alterations while concomittantly preventing gastric aspiration and reducing noscomial pneumonia could be better optimised.

It is also noteworthy that current widespread practice to rely on the ability to inflate ETT cuffs to a safe pressure, as well as to detect overinflated ETT cuffs by mere palpation of the ETT pilot balloon is unsafe for patient and medically unethical. Pressures must be monitored by a pressure manometer.

Conflict of Interest:

None declared