Most infants with congenital heart disease undergoing reparative surgery need post op ventilatory support for variable periods. An increasing density of infant tracheostomies force me to ask " What is a Tracheal function test?" How do we assess whether the trachea has healed and is ready or has become malacic after intubation?
This is a complicated question. There are many issues. Placement of a trach often causes a loca lextra-thoracic tracheomalcia defined as cartilage deformaton and collapse narrowing the airway around the trach, causing a stenosis. This is probably multifactorial but included compression form the tracheostomy tube.Often granulation tissue will form as well, further narrowing the airway, or even blocking it. These issues are best diagnosed at bronchoscopy. The intrathoracic trachea can develop tracheomalacia as well from the tracheostomy from chronic inflammation. Tracheomalacia defined as cartilage deformation may have been present before the trach was placed, and may worsen. In addition, there may be excessive posterior membrane dynamic intrusion that worsens the airflow. This can be diagnosed at rigid or flex bronchoscopy during very active breathing. Particularly vulnerable is the left mainstem bronchus that can get compressed between the pulmonary artery and the descending aorta. Children with congenital heart disease can have much more complex tracheal issues such as vascular ring and slings. This is a huge topic for a simple question.
Thanks, Jennings for the thought....i am seized with the issue and needed to do something about it . Was more specifically interested in the "flow dynamics" and related growth of the lung bud in utero whence the amniotic fluid flow facilitates the trach growth and bifurcation...what happens ex utero when we give large flows (>10-15l/mt) of air/gases through a tracheostomy in an infant/ neonate? Are there any animal models/ mathematical models? Worth a study , i guess...couldn't find answers in Gray's or Guyton's..:)
PS: the headdress is funny and looks Indian...! just kidding
Thanks for the reply,anyways
Sorry, Dr.Jennings,
Your profile pic shows a cap like an Indian Prince's crown ....and the color matched too.... i didn't mean to be offensive! apologies
PS:AM going through your conf papers and would discuss further after reading them.
Ramesh
In utero the gentle postive pressure created by lumg fluid production before 32 wwek gestation or so leads to gentle distention and lung development and growth. If you remove teh distention pressure with a hole in teh airway, the lung develops less. If you obstruct the lung fluid outflow, the lung devleops larger. I think after birth, the dynamic are different. In that case, one does want to damage any alveoli, while letting them grow, but one must distend them and get oxygen exchange. Overdistnation can damage teh alveoli.
".......one does want to damage any alveoli, while letting them grow, but one must distend them and get oxygen exchange." I guess you meant , one does NOT want to damage any alveoli; and its a typo!
But what happens to Trachea /tracheal function with the flow of air (instead of amniotic fluid)....Does it respond similar to in utero?
How did you convince the surgeons about aortopexy ...because in our institution , the sternum is left open for a period of time in ASO for dTGA and then tracheostomy is done if there is TBM?
the posterior membrane intrusion in intrathoracic TBM is countered with the Trache Tube(theoretically)
the same child (infant with Cong.Diaphragmatic hernia) is on ECMO + HFO . how does one assess the airway compliance/ resistance in such complex situations.....how to begin thinking "hitting the ground running" when seized of such matters!
there should be an artistic way out!
Cheers and Thanks
Ramesh
The aortopexy elevates the anterior wall of the trachea based on the attachments of the trachea to the aorta. Anterior tracheaopexy will directly elevate the anterior tracheal wall. Neither of these addresses the posterior intrusion - what is called excessive dynamic airway collapse in the adult literature. Wheh the trachea is displaced anteriorly, the posterior intrusion may be less, or it may be the same becasue the lung slips into the "space" and continues to push the posterior membrane anteriorly. Fpr thises reasons, we have developed the techniques for posterior tracheopexy, and have been quite satisfied with the outcomes. I hope this helps. Rusty
Hello Dr.Jennings,
Season's greetings
I am still with the tracheal dynamic modulus study and am interested in knowing your thoughts on the tracheal / bronchial buttressing with some sort of scaffolding. we have lot of baby's with Down syndrome / AVSD who get operated and end up with airway / bronchomalacia requiring prolonged tube (endotr or Trache) . Our ENT colleagues are gracious enough to accommodate them in their Trache clinic but decannulating these young infants is a loong and miserable journey for the entire team.
Awaiting your insightful comments
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