Tubercular mediastinal lymphadenopathy: An unusual cause of failed decannulation and tracheostomy.

Literature has described many causes of failed decannulation and weaning. However, failed decannulation and weaning from ventilator due to a hilar lymph node compressing upon a bronchus has not been described. We report a case of a 30-year-old man with Guillain-Barré syndrome who had quadriparesis and respiratory distress. After 1 year of intensive care unit admission, he was ambulatory, haemodynamically stable, devoid of sepsis, had effective cough with tracheostomy in situ. Every attempt of decannulation led to pooling of secretions in left side of chest, hypercarbia and altered sensorium. This was followed by re-institution of ventilator support. Chest x-ray was unremarkable, but computed tomography (CT) chest done during this time showed a mass compressing upon left lower lobe bronchus. Flexible fibre-optic bronchoscopy and transbronchial biopsy confirmed the diagnosis to be tubercular lymph node. After 1 month of starting of anti-tubercular treatment, there was resolution of the mass with relief of the bronchial compression and a successful decannulation thereafter. Role of CT in difficult cases of weaning is emphasized, and role of bronchoscopy is highlighted in difficult cases of weaning and decannulation.

INTRODUCTION

Decannulation of a patient with prolonged tracheostomy is not a straightforward task, the most common causes of failure being retained secretions and inability to produce effective cough due to respiratory muscle fatigue, abnormal ventilatory drive, or another episode of respiratory failure.[1] We encountered tubercular mediastinal lymphadenopathy (TML) as an unusual cause of multiple failed decannulation in a patient of Guillain-Barré syndrome (GBS). We believe that this has not been described earlier.

CASE REPORT

A 30-year-old, conscious, afebrile, tracheostomised man with quadriparesis and respiratory insufficiency was referred to our intensive care unit (ICU). After initial ventilator support of synchronized intermittent mandatory ventilation/assist-controlled breathing (SIMV/ASB), the patient was gradually weaned over a period of 1 year. During this period, the patient had multiple episodes of ventilator-associated pneumonia and was treated according to culture sensitivity reports, along with conventional pharmacological management for GBS. Once quadriparesis improved, the patient was given T-piece trial everyday, with increasing time durations in subsequent trials. After ensuring a vigorous cough reflex, absence of respiratory infection, stable haemodynamics, normal chest radiographs and normal arterial blood gases, a trial of decannulation was started in accordance with standard protocol and criteria of decannulation.[2] The patient's trachea was decannulated, and the patient was shifted to the ward. However, 1 week after decannulation, the patient was re-admitted to ICU with complaints of loss of consciousness, diaphoresis and deranged arterial blood gases (ABGs) with pH of 7.20, pCO2 of 14.79 kPa, PO2 of 22.48 kPa, HCO3 of 36 mmol/L, base excess of –9.0 mmol/L and SaO2 of 98% at FiO2 of 0.5% with no evidence infection. Auscultation revealed coarse crepitations on left side of chest. Patient's trachea was re-cannulated, and the patient was mechanically ventilated with SIMV/ASB mode after tracheal suctioning. The patient was again weaned down to T piece; and later, on room air with clear chest and normal ABG, he was decannulated for the second time. Surprisingly, 8 to 10 days later, the patient had to be re-cannulated due to a problem similar to the one described above. This entire cycle of decannulation and recannulation occurred 3 to 4 times.

With every subsequent attempt of decannulation, the patient complained of heaviness, inability to clear secretions from the left side of chest and persistent hypercarbia but without hypoxia. A flexible fibre-optic bronchoscopy (FFB) was done at this stage, and it showed a slit-like opening in the left lower lobe bronchus with a normal-appearing mucosa distally [Figure 1]. An externally compressing mass was suspected and was confirmed in the computed tomography (CT) of chest [Figure 2a], which also revealed segmental collapse consolidation of left postero-basal lung. A transbronchial needle aspiration of the lymph node mass confirmed diagnoses of tuberculosis in the form of epithelial cell granuloma, Langhans type of giant cells and acid-fast bacilli (AFB). Tracheal cultures, however, were negative for AFB. A course of Antitubercular treatment (ATT) was started, and improvement in the general well-being of the patient was evident within a week. A follow-up CT chest [Figure 2b] after 1 month of commencement of ATT showed significant regression of the lymph node mass and an increase in the calibre of the left lower bronchus. The patient's trachea was successfully decannulated after 2 weeks of treatment, and the patient never required recannulation thereafter. He was subsequently discharged home after a stay of further 2 weeks in the ward.

Figure 1

Flexible fibreoptic bronchoscopy of left lower lobe visualizing an external compressing mass (1) and a slit-like opening in left lower lobe bronchus lumen (2) A transbronchial aspiration needle can also be seen (N)

Figure 2a

Computed tomography of chest showing an externally compressing mass (1) slit-like opening in left lower lobe bronchus lumen (2) and segmental collapse consolidation of left postero-basal lung (3)

Figure 2b

Regression of the lymph node mass (1) with increase in the calibre of the left lower bronchus (2) and a normal lung (3)

DISCUSSION

GBS is an autoimmune disease of peripheral nerves, with 80% of the patients recovering within a year.[3-4] During recovery, surviving axons send collateral sprouts to muscle fibres, which results in decreased efficiency and easy fatigability during weaning.[3] Initially the cause of failed decannulation was attributed to GBS; however, in an ambulatory patient with no evidence of active infection and requiring multiple re-admissions, further evaluation was necessary.

Tuberculosis is endemic in this part of the world. Reactivation of TML in an immune-compromised host is a real possibility, which usually peaks at 20 to 40 years of age with no systemic symptoms.[5] The most common form of extra-pulmonary tuberculosis is tuberculous lymphadenopathy, and its diagnosis remains a challenge.[6-7] CT is invaluable in assessing hilar and mediastinal pathologies which are often poorly characterized in plain radiography.[3]

The ineffective clearing of secretions from the left side of chest and subsequent hypercarbia could be explained due to dynamic compression of the intra-thoracic narrowed portion of lower lobe bronchus during coughing. The dull aching pain in left lower chest could possibly be related to an increase in capsular stretching of the enlarged lymph node. Other causes of lymphadenopathy were also ruled out clinically and histopathologically.[3] Patients on prolonged ventilation develop critical induced polyneuropathy, which cannot be completely ruled out as no nerve muscle conduction study was possible; but it is rarely present in isolation,[4] and patient's clinical response to ATT rules it out even further.

In conclusion, TML and mediastinal pathology should be considered as a possible cause of failed decannulation of trachea. The roles of CT chest and FFB are invaluable in clinching these pathologies.