Weaning from prolonged mechanical ventilation: The complete picture

Sir,

I read with interest the article by Thapa D et al. titled “Tubercular mediastinal lymphadenopathy: An unusual cause of failed decannulation and tracheostomy”[1] published in the Indian Journal of Anesthesia (2011; 55:293-5).

The authors deserve rightful credit and appreciation for a clear and succinct report and an interesting observation with a possible unusual cause for the decannulation failure. However, I was a part of the institution at the time of this case scenario, and being personally involved with care of the patient in question, I would like to highlight some more pertinent issues in the weaning failure that may have been overlooked by the authors.

The case report pinpoints the tuberculous lymphadenopathy and consequent non-clearance of secretions with possible underlying lung collapse as the cause of failure to wean.[1]

However, these are a few other clinical issues that might have contributed to weaning failure:

• A)Moderate grade with a regurgitant fraction of 20-30% or 2+ on transthoracic echo.
• B)He was in the intensive care unit (ICU) for a period greater than 15 months, of which >12 months were spent on mechanical ventilation.
• C)Lack of adequate oral nutrition – prolonged period of tube feeds for a period greater than 12 months.
• D)Polypharmacy in the ICU, namely prolonged use of steroids, neuromuscular blockers (initial period) along with IV antibiotics for greater than 12 months and periods of electrolyte imbalances, which required correction.

The complete picture thus is of a severely deconditioned male who presented to us with ascending polyneuropathy (possible guillain-barre syndrome (GBS)). Over a period of fifteen months of ICU stay, he became progressively more deconditioned, despite our best efforts to work on his nutrition and physical rehabilitation. The neurological insult prevailed for at least six months before recovery began, and was very slow. In the interim, the mitral valvular lesion was discovered as an incidental finding. The prolonged use of steroids and neuromuscular blockers could also have contributed to myopathy and neuropathy. On close analysis, it is obvious that challenging such a patient with an acute increase in the work of breathing (as in repeated decannulation attempts) called on extra cardiovascular reserves and strength of the intercostals and diaphragmatic musculature, which he lacked, and consequently failed successful weaning. In addition, the lymphadenopathy in question was most definitely chronic and asymptomatic and existed prior to the GBS. There is no reason why an asymptomatic lesion such as this can be blamed all by itself for a decannulation failure.

There is enough literature that has been cited time and again that has emphasized that weaning failure in the ICU is seldom attributable to a single problem.[2,3] Drug-induced myopathy, neuropathy, muscle wasting in the setting of nutritional deprivation and, most importantly, co-existing cardiac disease (especially regurgitant lesions) are the most common offenders that need to be looked at. In combination, these factors can cause respiratory pump failure and left ventricular dysfunction, which is enough to tip the balance in favour of an unfavourable outcome at weaning attempts. I believe that the successful decannulation in this case report after treatment of the possible culprit lymphadenopathy is a co-incidental occurrence with not enough evidence to prove a temporal cause and effect relation. Agreeably, the lymphadenopathy could have been one of the contributing factors in this scenario, but it was only another piece in the puzzle!

Intensivists and critical care physicians need to adopt a more wholesome approach while tackling weaning failure.