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 Table of Contents  
Year : 2017  |  Volume : 4  |  Issue : 2  |  Page : 93-95

Congenital tracheal stenosis challenging the management of patent ductus arteriosus in an infant

1 Department of Anaesthesia and Intensive Care, Postgraduate Institute of Medical Education and Research, Chandigarh, India
2 Department of Cardiothoracic and Vascular Surgery, Postgraduate Institute of Medical Education and Research, Chandigarh, India

Date of Submission12-Nov-2015
Date of Acceptance20-Mar-2017
Date of Web Publication12-May-2017

Correspondence Address:
Banashree Mandal
Department of Anaesthesia and Intensive Care, Fourth Floor, A Block, Nehru Hospital, Postgraduate Institute of Medical Education and Research, Sector 12, Chandigarh - 160 012
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/roaic.roaic_58_15

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Congenital tracheal stenosis (CTS) has an incidence between 0.3 and 1% of all laryngotracheal stenosis [1]. In about 84% of such cases, it is associated with cardiac, skeletal or oesophageal anomalies. The associated cardiac anomalies include ventricular septal defect, atrial septal defect, patent ductus arteriosus, atrioventricular canal defect and pulmonary artery sling [2]. The diagnosis of CTS is based on high degree of suspicion in infants with respiratory distress. Classically, infants have a stridor that is exacerbated by lower respiratory tract infection and present with intermittent cyanosis, leading to reflex apnoea or dying spells. A 1 mm decrease in the cross-sectional area (CSA) of the airway results in 44% decrease in CSA. Infants become symptomatic only when the decrease in CSA is more than 50% and become dyspnoeic when the CSA decreases by more than 75% [3]. We present the hospital course of an infant who presented with CTS and a large patent ductus arteriosus. The present case is reported with parental consent.

Keywords: congenital tracheal stenosis, infant, patent ductus arteriosus, pulmonary hypertensive crisis

How to cite this article:
Mandal B, Mishra AK, Batra YK. Congenital tracheal stenosis challenging the management of patent ductus arteriosus in an infant. Res Opin Anesth Intensive Care 2017;4:93-5

How to cite this URL:
Mandal B, Mishra AK, Batra YK. Congenital tracheal stenosis challenging the management of patent ductus arteriosus in an infant. Res Opin Anesth Intensive Care [serial online] 2017 [cited 2023 Mar 26];4:93-5. Available from: http://www.roaic.eg.net/text.asp?2017/4/2/93/206155

  Case report Top

A 5-month-old male infant weighing 5 kg presented to the Paediatric Emergency Department of our hospital with cyanosis and apnoea [1],[2],[3]. Cardiopulmonary resuscitation (CPR) was performed, and the infant was resuscitated and intubated. After CPR, he had stable haemodynamics and a Glasgow coma scale (GCS) of E4VTM6. He had significant past history of similar episodes of apnoeic spells and cyanosis since 1 month of age (at least one episode every month). On investigation, his biochemical parameters were within normal limits except for haemoglobin of 8 g% and total leucocyte count of 24 000. A two-dimensional transthoracic echocardiography demonstrated 5.4-mm patent ductus arteriosus (PDA) with left-to-right shunt, a tiny muscular ventricular septal defect, right-sided aortic arch and right ventricular systolic pressure=right atrial pressure+26 mmHg. As the clinical condition was not corroborating with the symptomatology of the infant, a chest computed tomography was performed to rule out any other anomaly. The computed tomography showed a tracheal narrowing adjacent to the PDA and collapse and consolidation of the right lower lobe of the lung ([Figure 1]). A working diagnosis of tracheobronchomalacia secondary to compression by the large PDA was made, and a bronchoscopy was planned; however, it could not be performed due to unavailability of a paediatric fibre optic bronchoscope. Two days later in the Emergency Department, the infant again had bradycardia for which CPR was performed. After resuscitation, he had stable haemodynamics with a poor GCS of E1VTM1. A neurology consultation ruled out any hypoxic damage to the central nervous system. Because of urgency of repair, he was referred to the Cardiothoracic and Vascular Surgery Department for surgical correction of congenital tracheal stenosis (CTS) and PDA. He was sedated with infusion of morphine and midazolam, as a struggling infant may precipitate tracheal collapse and precipitate obstruction. The patient was shifted to the Cardiothoracic and Vascular Surgery ICU and kept on intermittent positive pressure ventilation [endotracheal tube (ETT) 4-mm external diameter, fixed at 12 cm at angle of mouth] with FiO2 100%. The infant’s arterial blood gases (ABG) were within normal limits. There was improvement in GCS to E1VTM4.
Figure 1 Computed tomography of chest showing lower tracheal narrowing

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In view of a large PDA and need for repair of the associated tracheal stenosis, PDA division was performed under cardiopulmonary bypass (CPB) the next morning ([Figure 2]). On external inspection, the trachea appeared normal but after the ETT it was pulled to a 10 cm mark at angle of mouth; the surgeon could identify narrowing of the lower trachea, adjacent carina and the right main bronchus. The narrowing was around 50%, but no abrupt tapering was seen ([Figure 3]); hence, the trachea was not intervened. The infant came off CPB without any inotropic support.
Figure 2 Suction tip showing the cut end of the patent ductus arteriosus

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Figure 3 Suction tip showing the carinal end of the dissected trachea

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After CPB, the infant was shifted to the ICU for postoperative elective mechanical ventilation around 1 p.m. Initially, the patient had high oxygen requirement with hypercarbia ([Table 1]). On postoperative day 0, serial ABGs showed improvement in oxygenation and normocarbia over the next 5 h. FiO2 was gradually reduced to 0.5. There was an episode of bradycardia and desaturation when ETT suctioning was performed at 6 p.m.; hence, suctioning was abandoned, FiO2 was increased and sedation with continuous infusion of morphine and midazolam was started. The patient remained haemodynamically stable with normal ABGs for the next 8 h, and as per routine care for such patients FiO2 was gradually tapered to 0.4.
Table 1 Serial arterial blood gases in cardiothoracic and vascular surgery ICU on postoperative day 0

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At 2.30 a.m. postoperative day 1, the infant had desaturation followed by bradycardia. Bag ventilation with 100% oxygen was performed after which the infant had 100% saturation. Shortly after that, the infant again had bradycardia and desaturation followed by cardiac arrest. CPR was administered; however, the infant could not be resuscitated.

  Discussion Top

In our case, the probable reasons for desaturation and bradycardia could be the following: (a) dynamic collapse of the lower trachea and inability to ventilate the lungs or (b) acute pulmonary hypertensive crisis, each leading to cardiac arrest. The current literature favours concomitant correction of both CTS and cardiac malformation in one setting [4]. If the cardiac anomaly is addressed without correcting CTS, the patient will have difficulty in weaning off the ventilator because of respiratory problems. On the other hand, if CTS is addressed first without addressing the cardiac anomaly, there is an increased risk for tracheal anastomotic dehiscence due to low perfusion caused by poor cardiac function. CTS management is based on symptomatology, anatomy of lesion, associated anomalies, etc. Bronchoscopy has a pivotal role in diagnosing the condition [2]. Different techniques are available for the treatment of CTS including surgery, laser, balloon dilatation and stenting [2].

In our patient, the symptomatology was highly indicative of a severe tracheal stenosis, but on physical examination the tracheal stenosis was only less than 50% of normal, allowing a 4 mm ETT. In infants, it is seen that a tracheal diameter of 4–6 mm is good enough for ventilation. Rutter et al. found good results with nonoperative management of tracheal stenosis with adequate diameter of 4–6 mm in small infants [5]. Hence, we planned not to touch the trachea. We could not rule out a dynamic component of tracheomalacia because of unavailability of fibre optic bronchoscopy.

Pulmonary hypertension (PAH) occurs in all intracardiac shunts with increased pulmonary blood flow, and the outcome after closure of a large PDA is determined primarily by age at the time of repair and pulmonary vascular disease [6]. However, the incidence of PAH in infants with PDA or ventricular septal defect is very low except for infants with Down’s syndrome [7]. However, the postoperative ICU course in our patient indicated an acute PAH crisis, as suggested by the infant having bradycardia and desaturation on ETT suctioning, which improved with hand bag hyperventilation with 100% oxygen. Again high-pressure bag ventilation might have helped stenting the lower trachea to maintain its patency until the infant was sedated and ventilation was controlled. The case management would have been better with (a) bronchoscopic delineation of the dynamic nature of tracheal stenosis, (b) cardiac catheterization to check for vasoreactivity of the pulmonary vascular bed, (c) invasive monitoring with Pulmonary artery (PA) line or Left atrial (LA) line, which could have allowed a timely recognition and management of PA crisis, (d) EtCO2 monitoring, which could have acutely differentiated between a tracheal collapse or PA crisis, and finally (e) advancement of the ETT to 12 cm depth, which could have worked as a stent to the lower trachea showing features of tracheomalacia.

  Conclusion Top

Management of infants with CTS and associated anomalies is complex and requires close cooperation between the paediatrician, cardiac surgeon, anaesthesiologist and nursing staff. Infants with CTS and associated intracardiac shunt should be cautiously managed postoperatively. Acute PA crisis as well as the dynamic nature of CTS should always be kept in mind during differential diagnosis while treating patients who present with desaturation and bradycardia.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Matate JA, Anton-Pacheco JL, Berchi FJ, Vilarino A. Lesiones-estructurales obstructivas tracheobronquiales. In: Valoria JM, editor. Cirugia pediatrica. Madrid: Ediciones Diaz de Santos; 1994. pp. 796–806.  Back to cited text no. 1
Juan LA, Indalecio C, Juan C, Lorenzo G, Polo L, Aracili G et al. Management of congenital tracheal stenosis in infancy. Eur J Cardiothorac Surg 2006; 29:991–996.  Back to cited text no. 2
Lalwani A. Current diagnosis and treatment in otolaryngology. 2nd ed. New York: Mc Graw-Hill Medical; 2007.  Back to cited text no. 3
Tsvetomir L, Christian S, Wolfgang S, Herbert U, Siegfried H. Simultaneous management of congenital tracheal stenosis and cardiac anomalies in infants. J Torac Cardiovasc Surg 2005; 130:1537–1541.  Back to cited text no. 4
Rutter MJ, Wiliging JP, Cotton RT. Nonoperative management of complete tracheal rings. Arch Otolaryngol Head Neck Surg 2004; 130:450–452.  Back to cited text no. 5
Bando K, Turrentine MW, Sharp TG, Sekin Y, Aufiero TX, Sun K et al. Pulmonary hypertension after operation for congenital heart disease: analysis of risk factors and management. J Thorac Cardiovasc Surg 1996; 112:1600–1607.  Back to cited text no. 6
Blount SG, Vogel JH. Pulmonary hypertension. In: Moss AJ, Adams FH, editors. Heart disease in infants, children & adolescents. Baltimore: William and Wilkins; 1968. p. 947  Back to cited text no. 7


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1]


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