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Wheezes and stridor (Part II)

As discussed in part – I, wheezing is common manifestation of respiratory illness and stridor is not uncommon too. To find stridor and wheezing is an art within science and its recognisationmakes a huge impact on management.

 Though asthma and COPD are most common causes, the causes of wheezes & Stridor are generally categorized based on their location.

  1. Extra thoracic upper airway causesinclude Anaphylaxis, Vocal cord edema, laryngeal stenosis, goiter etc. Paradoxical vocal cord motion (PVCM)is an important but often over looked cause. (See the discussion below).
  2. Intra thoracic central airway causesinclude Tracheal stenosis, Tracheal and bronchial tumours, tracheobronchomalacia, relapsing polychondritis and mediastinal masses. Tracheobronchial amyloid is rare but significant morbidity related cause of Wheeze (See discussion below)
  3. Intra thoracic lower airway causesinclude Asthma, COPD, Bronchiolitis and Cardiac Asthma. However carcinoid tumour (see discussionbelow) and air way distortion due to TB (see discussion below) are significant causes of wheeze and stridor in India.



Carcinoid tumor right main bronchus


Left Main Bronchus Post Tubercular Stenosis


Post tracheostomy stenosis



Big multiple nodules in right main bronchous suggesting lung amyloid


Adducted vocal cords in inspiration (PVCM)

  1. For patients with rapid onset of respiratory distress, key initial steps are to ensure adequate oxygenation and ventilation based on pulse oximetry and arterial blood gas measurement, followed by a rapid assessment made to determine the most likely cause. If asthma and COPD are likely, nebulized bronchodilator treatment is immediately given. If there is evidence of anaphylaxis, subcutaneous epinephrine should be given immediately.
  2. For patient with impending respiratory failure (i.e. impaired oxygenation by pulse oximetry, increased arterial tension of carbon dioxide) and suspicion of central airway obstruction, endotracheal intubation by an experienced clinician should precede a diagnostic evaluation if the initial measures have failed to improve the situation. For severe tracheal obstruction, use of an open ventilating rigid bronchoscope may be necessary. In these patients, the diagnostic evaluation proceeds concomitantly with steps to provide adequate ventilation.
  3. For the patients with a stable respiratory status, a carful history and physical examination may narrow down the potential causes of wheeze, not due to asthma or COPD.
  4. For most stable patients, the initial pulmonary function test is spirometry before and after inhaled bronchodilator. For patients who do not meet criteria for asthma or COPD or do not respond appropriately to the trial of bronchodilator and anti-inflammatory medication, a careful examination of the flow volume loop is in order. The flow volume loop can be used to help determine whether the obstruction is fixed or variable and whether it is likely to be intrathoracic or extrathoracic.

Imaging of the neck and chest (eg, conventional chest and neck radiographs, computed tomography (CT), three-dimentional reconstruction CT, end – inspiratory and expiratory CT) plays an important role in the evaluation of wheezing due to structural lesions in the central airways.

Direct visualization of the airway is often necessary to make a definitive diagnosis of the causes of wheeze,where central airway obstruction is suspected. At the time of visualization, biopsies can be obtained of intraluminal masses and plaques.

Paradoxical vocal cord motion: It refers to inappropriate movement of vocal cords. It has been associated with psychological disorder, stress, exercise, neurological injury and perioperative airway. The glottic aperture is obliterated except for a posterior diamond shaped passage.

Tracheobronchial amyloid:Amyloidosis is deposition of abnormal proteins in extra cellular tissue. Lung Amyloid presents like parenchymal nodule or tracheobronchial nodules. Clinically it has wide variety of presentation like an accidental CT finding to progressive un responsive Wheeze and stridor.

Carcinoid tumour:These are fascinating but uncommon group of pulmonary neoplasms. Previously labelled “Bronchial adenoma “sounds a benign nature doesn’t hold true. It’s a spectrum of neuro endocrine tumours that includes small cell carcinoma as its most malignant member. They are found in cartilaginous portion of trachea bronchial tree and are attached to bronchus by broad base or with a distinct stalk. They are highly vascular and usually are covered with intact epithelium.


Air way distortion due to TB: Despite rapid advancement in diagnostic and therapeutic modalities, endobronchial TB, continues to remain challenging. Non Specific symptoms, focal wheezes, stridor and normal chest X Ray delays the diagnosis. Bronchoscopic biopsy is most reliable diagnostic tool in almost 84% of cases. Progression to stenosis is not uncommon and early intervention like balloon broncoplasty is essential to halt the natural course.


1 Paradoxical vocal cord motion disorder: Past, Present , Future: Post Graduate Medical Journal 2007 Mar;83(977):164 – 172, Wanis Ibrahim, HeithamGheriani.

2 AL Amyloidosis: Case report: JAPI, Oct 2012.

3 Carcinoid Lung Tumours: Medscape Jan 15, 2017: Mery C Mancini, MD.

4 Challenges in endobronchial tuberculosis: from diagnosis to management: Pulmonary Medicine Vol 2014, Article ID 594806. Dr SurendraKashyape, Dr Anjali Solanki.

5 Evaluation of Wheezing illnesses other than asthma in adults: Peer review Up To Date : Jan 3, 2017: Richard S Irwin, MD.

Dr. Ajit Kulkarni

Consultant – Chest Disease,

Interventional Pulmonology & Critical care Medicine

Wheezes and Stridor (Part 1):

History: 80 years female was brought to our hospital at around 9 pm for severe breathlessness of 4 days duration. She was apparently all right 4 days before admission.She was known case of lymphoma and had received chemotherapy & radiotherapy (radiation for neck lymph nodes)and was declared cured (?).

Rapid evaluation showed exhausted old lady with sweating. She was tachycardic and tachypnoeic. She could not tell her name completely (marked techypnoea but no hoarseness). Auscultation for lung reveled stridor and high pitched wheezes more prominently on trachea. An attempt for Noninvasive ventilationby CMO drastically failed and she became more hypoxic.  Her Chest X Ray & ECG were normal and quick bed side 2 D Echo did not show Reginal Wall Motion Abnormalityor Pulmonary Embolism.

We did quick bronchoscopic examination immediately (bedside in ICU)in view of clinically suspected intra thoracic major airway obstruction.

It revealed major mid tracheal obstruction by an exophytic growth occluding > 80 % of lumen. We did emergency bronchoscopic intubation after gentle coring of the mass and pushing Endo Tracheal Tube beyond the mass. Position of tube was ascertained (1cm above carina) by check bronchoscopyafter 5 mins and was ventilated. She survived the catastropheand became fully alert in the morning. An High Resonance CT Scan,next morning, showed reappearance of masses in the mediastinum with erosion of trachea.

Patients herself and relatives denied second line treatment for lymphoma and METAL TRACHEAL STENTING. What was left with us was to put MONGTOMARY TUBE or TRACHEOSTOMY TUBE with longer length.


Her Ventilator was removed immediately.She settled with spontaneous breathing without respiratory distress. With proper tracheostomy care, taught to the relatives, she was discharged from the hospital on 5thDay.

part1Exophytic Mass in Trachea                                   part2T’ stomy Tube Beyond mass

Discussion:Wheezing is a common manifestation of respiratory illness in adults. Though wheezing indicates, asthma or COPD, wheezing is also caused by spectrum of other processes that cause airflow limitation.”All that wheezes is not asthma (or COPD), all that wheezes is obstruction”

Wheezes are usually high pitched, mono or polyphonic; occur during inspiration or expiration (more in expiration) while stridor refers to a monophonic sound typically in inspiration heard over trachea.Quick auscultation over trachea to find stridor and wheezes is an art within science. It makes a huge difference in management protocols viz. bronchodilator and surgical airway management.

The causes of Intra thoracic airway obstruction are many, which includes simpler one like mucus plug to tracheal stenosis, tracheal and bronchial tumors, mediastinal masses, respiratory papilomatosis or tracheo bronchomalacia.

Evaluation of wheezy patient in respiratory stress is challenging. Supplemental oxygen, Bronchodilators, Steroid are important for patients with impending respiratory failure and with strong suspicion of central airway obstruction, quick control over airway is mandatory. Failing to do so, may end up with disastrous outcome.


  1. Evaluation of Wheezing illnesses other than asthma in adults: Peer review Up To Date: Jan 3, 2017: Richard S Irwin, MD.
  2. Fundamentals of Lung auscultation, NEJM, 2014: 370:744
  3. Excessive dynamic airway collapse. Respirology 2006;11:388

Dr Ajit Kulkarni

Consultant – Chest Disease,

Interventional Pulmonology & Critical care Medicine

60 yrs female was suffering from adenocarcinoma of left lower lobe bronchus with multiple metastasis. Palliative chemotherapy gave her good quality life for 8 months. She came back with breathlessness to have left massive pleural effusion. Diagnostic thoracoscopy showed multiple metastasis. Pleural effusion was drained and pleurodesis was done (with steritalc) in same setting. It resulted in good pleural thickening and symptomatic relief.







It is not known why human evolved to have a pleural space. Elephants do not have pleural space and do not have adverse effects. It is thought that their lack of pleural space prevents paranchymal injury during snorkeling. Presence of fluid, air in pleural space affects lung, chest wall and cardiovascular system. Patients with pleurodesis do not suffer adverse respiratory problems from their lack of pleural space.

Definition and Mechanism of Action:

Pleurodesis is defined as symphysis of parietal and visceral pleura. The fibrosis is caused by fibrin production of parietal pleura, as a reaction to inflammation, which in turn caused by chemical or mechanical agents. The most common indication for pleurodesis are malignant pleural effusion and pneumothorax. It may be indicated in some benign conditions like CKD, Hepatic pleural effusion.

Sclerosing agents used for chemical pleurodesis are talc, bleomysin, tetracycline and iodopovidone (10%). Amongst all the agents, talc pleurodesis has high success rate upto 90% even in first setting.

There are two different techniques of intra pleural administration of talc

  1. Insufflation of dry talc powder into chest cavity during thoracoscopy. This is performed in operation theatre under local or general anesthesia.
  2. Other technique is administration of talc slurry through a chest tube.

Though there is no significant difference in recurrence rate between the two, a large prospective randomized trial showed talc poudrage more efficient in the sub group of breast and lung cancer with the success rate of 82% against 67% for talc slurry.

Two important issues needs to be considered in this procedure. First, initial therapeutic thoracocentesis should relieve the dyspnoea of patient and complete re-expansion of lung and second, particle size of talc powder. Small particle size of talc or medical talc without known particle size is likely to produce more lung inflammation and complicate the situation.



  1. Principles and practice of Interventional Pulmonology: Armin Ernst: 623-629
  2. Dresler CM, Olak J et al: Phase III inter group study of talc pouderage vs talc slurry in malignant pleural effusion. Chest. 2005; 127: 909-15
  3. Das SK, Saha SK: comparison of efficacy and safety of talc and iodopovidone for pleurodesis. J Indian Med Assoc. 2008; 106: 589-90


Dr. Ajit Kulkarni

Consultant-Chest Disease, Interventional Pulmonology,

Critical Care Medicine



Case History:

25 years girl was referred for progressive breathlessness and was restless at rest. She was treated with ventilatory support after tracheostomy for her G.B. syndrome. Became well, tracheostomy closed and was discharged. She became breathless after third day of discharge. Clinically, she had stridor. Her CT chest showed tracheal stenosis (web like stenosis) and hence was referred.

Emergency bronchoscopy examination showed tracheal stenosis (75%). In same setting, she was subjected for balloon bronchoplasty with electrocautery to cut the web. I also installed local steroid. Trachea was fully opened with complete symptomatic relief. The procedure was done under general anesthesia with use of I-gel instead of intubation. She was discharged within 16 hours.



Non malignant airway obstruction covers many pathologies that differ from malignant diseases. Common obstructions are post intubation/tracheostomy stenosis (scar) post tubercular fibrosis or web (scar). Wegener’s granulomatosis or sarchoidosis (intra luminor stenosis) or tracheomalacia (dynamic obstruction).

The clinical presentation depends on severity of obstruction and on cardio pulmonary reserve. Typically, patients remain asymptomatic until stenosis exceeds 50%. Symptoms at rest only present when tracheal lumen narrowing is <5mm.WHEEZING REFRACTORY TO BRONCHO DILATOR THERAPY IS CLUE TO THE DIAGNOSIS. A high index of suspicion is needed if the patient presents with history of prior intubation, tuberculosis, GE reflux or systemic illness like wegener’s. CT scan chest provides valuable anatomical information on location, type, extent of lesion. Spirometry may yield classical F/V loop but used sparingly because of demanding nature in distressed condition.


(Web like tracheal stenosis)


(Balloon bronchoplasty)


(Electrocautery cut)


(Final result)

Post intubation/tracheostomy stenosis is common cause of benign traceo stenosis followed by tuberculosis.

Web like stenosis are treated endoscopically with laser/electrocautery resection and dilatation achieving success rate of 70-95%. A mucosal sparring technique should be used to preserve as much normal mucosa as possible. This involves making radial incision with laser/cautery at 3, 9 and 12’o clock position. There are two broad categories of tracheal dilatational techniques rigid bronchoscopy barrels or semi rigid bougie dilators. Alternatively salin or contrast filled balloon dilation is attempted and has gained more popularity.


  1. Principles and practice of Interventional Pulmonology: Ermin Ernst, Felix J.F. Hearth: 269-283
  2. Chhajad P.N. B, Brutsehe M. Balloon Dilatation using flexible bronchoscopy for the management of benign and malignant airway stenosis. Chest 2004; 125(1): 354-5
  3. Mehta A.C., Lee FY et al. Concentric tracheal and subglottic stenosis: management using Nd-YAG laser for mucosal sparing followed by gentle dilatation. Chest 1993;104:673-7


Dr. Ajit Kulkarni

Consultant-Chest Disease, Interventional Pulmonology,

Critical Care Medicine



Case History:

59 years male was referred to me for admission in ICU for non responding breathlessness. He was heavy smoker (60 pack years) and was diabetic. Breathlessness had worsened in 5 days after brief episode of fever. Past history revealed attacks of mild haemoptysis for nearly 6 months and history of intermittent hoarseness of voice which used to recover spontaneously.

He was treated on the lines of resistant COPD and was worked up on the same lines including HRCT Chest, ABG, 2D Echo, PFT etc. Because his rhonchi did not improve and HRCT showed a nodule in right lower lobe of lung, bronchoscopy was performed. Bronchoscopy yielded extensive nodularity right from trachea to lower lobes. The nodules in right lower lobe had completely occluded the lumen. Biopsies of multiple nodules were taken and were subjected for HPE. H & E staining showed extensive deposition of pink amyloid material in lamina propria. We further evaluated the slides with congo red staining which confirmed the diagnosis of lung amyloid. His work up did not show involvement of kidneys (No proteinurea) and bone marrow was normal hence confirmed the diagnosis of primary lung amyloidoisis, a rare diagnosis with poor prognosis.


(Nodule in Right Lower Lobe)


(Bronchial wall nodules)


(H & E stain showing amyloid)


Amyloidosis is a disease characterized by deposition of abnormal proteins in extracellular tissue. The deposits may originate from serum or are locally produced.

Amyloidosis may be “Systemic” (multiple anatomic site deposition) or “localized” (one anatomic site deposition). The term “Secondary” used to describe patients with co-existent disease like multiple myeloma and “Primary” for patients with no such co-existent disease.

Most pulmonary amyloidosis is associated with systemic amyloidosis. Almost 80% of pulmonary amyloid has systemic amyloidosis and 88% of systemic amyloid find pulmonary amyloid on autopsy.

Lung amyloid presents with various patterns like paranchymal nodule or tracheo bronchial nodules. It may present as diffuse alveolar septal type or adenopathy. Clinically it has wide variety of presentation like an accidental finding on CT scan to progressive unresponsive breathlessness.

Depending upon the protein fibrin deposition Amyloidosis is labelled as AL type or AA type. Common amyloid depositions are AL type. However, the difference in type of amyloid deposition does not make any change in progress of disease or treatment.

Localized amyloidosis are characterized by benign course and are not associated with systemic amyloidosis. Despite its localised nature, tracheobronchial amyloid may result in significant morbidity due to obstructive phenomena. Lung amyloid associated with primary systemic amyloidosis presents as a diffuse interstitial pattern (D/D ILD) with or without plural effusion. Complete survival data indicate that long term outcome is poor. Though nodules are likely to bleed, bronchoscopic lung biopsy is accepted as a safe and effective diagnostic technique.



  1. Smith RR, Hutchison GM : type & distribution of pulmonary amyloid,

AmJMed; 1977; 66:96-104

  1. Pulmonary amyloidosis The Mayo Clinic experience from 1980 to 1993

Ann Intern Med 1996 Feb 15: 124(4):407-430

  1. AL Amyloidosis : Case report : JAPI October 2012

Dr. Ajit Kulkarni

Consultant-Chest Disease, Interventional Pulmonology,

Critical Care Medicine



Case Summary:

58 yrs morbidly obese male was referred with H/O progressive breathlessness of 5/6 days duration. He was getting breathlessness for six months which eventually. He was managed with NIV (PC) and other measures for CHF management. His bedside echo showed RA/RV dilatation. CT pulmonary angiogram showed bilateral pulmonary artery emboli. In view of submassive PE, he was treated with LMWH, decongestive drugs, tadalafil and NIV.

He was subjected for polysomnography immediately after his crisis was over to evaluate OSA. He showed strong evidence of OSA and discharged with necessary CPAP dose adjustment.

(D shaped LV in Echo)


(Bilateral pulmonary emboli)


(Polysomnography showing OSA)


Management of dyspnoea by NIV – PPV has gained popularity in recent times. Though it is useful in hypercarbic respiratory failure, it is widely used in hypoxic respiratory failure with variable outcome. Most often we notice need of NIV for long time and these cases need further work-up viz. OSA.

Obstructive sleep apnea (OSA) is not a new concept. It does exist for more than 30 yrs now. Today, 13% population in India is under threat of OSA (Times of India, August 2, 2013) and 8% in patients admitted in ICU for various reasons (Mary Ann Moon, Oct. 20, 2014)

OSA cause systemic consequences due to hypoxia and endothelial dysfunction. Storm of mediator like TNA-alfa leads to upregulation of inflammatory cascade leading to multiple organ failures. Like chronic illnesses like hypertension, CAD, Stroke, insulin resistance, PCOD, acute illnesses like sudden death, massive pulmonary embolism are also under the grip of OSA.

The symtoms of OSA are quite non specific and include fatigue, day time hyper somnolesence, poor motivation, dozing while driving. These symtoms are ignored easily but these disorder needs to be focused more precisely in cases who present with its consequences like PE, CAD, CVA.

We keep strong suspicion of OSA in following conditions:

  1. Obese patient 2.Young age patient 3.Multiple systemic involvement 4.Hypercarbic respiratory failure 5.Hypoxic respiratory failure to respond 6.In difficult weaning from ventilator 7.In post operative stormy cases


  1. OSA – Obstructive Sleep Apnea
  2. NIV – Non Invasive Ventilation
  3. CPAP – Continuous Positive Airway Pressure (type of NIV)
  4. PE – Pulmonary Embolism
  5. LMWH – Low Molecular Weight Heparin


  1. Association of OSA and PE: Alonso Fernandes A;De La Pena M.

Mayo clinic proc. 2013 June, 88(8)579-87

  1. Snoring and risk of OSA in patients with PE:

Sleep, 2010 Aug, 33(8), 1069-74

  1. Mechanism of Endothelial dysfunction in OSA:

Vascular health and risk management, 2008 Dec, 4(6)1327

Dr. Ajit Kulkarni

Consultant-Chest Disease, Interventional Pulmonology,

Critical Care Medicine



 23 year female was referred to me with history of high grade fever and loose motions of 2 days duration followed by breathlessness and extensive areas of interstitial pneumonias.She was suspected to have H1N1 pneumonia with ARDS. On arrival initial workup for pneumonia including H1N1 and bacterial was done.

She was put on protocolised plan of treatment according to Tropical Infection Related Fever & Shock Protocol by ISCCM.

Her previous record showed history of body pains, persistent proteinurea and low WBC count for almost 1 year. She had history of abortion in first trimester of her pregnancy last year.

Her tachypnoea rapidly worstened and was electively ventilated, Also needed immediate SLED support for failing output (RIFLE CRITERIA). Her WBC, platelet count and Hb remained low hence bone marrow study done on day 2 of admission and antibiotic strategy was escalated like febrile neutropenic patient.

Bone marrow was done with suspected diagnosis a) Aleukaemic Leukemia b) B cell Lymphoma.

Surprisingly Bone marrow report was strongly suggestive of Haemophagocytic Syndrome (Macrophage Activation Syndrome).

(On Admission)



(After 4 Days)



(Macrophage showing Engulfed RBC & WBC)

She was put on I/V methyl prednisolone. She started improving and all her supports including ventilator, SLED, vasopressors were removed in 3 days time. She was given I/V Rituximab 325 mg / sq.m as addition biologics to steroid. Her WBC count persistently remainedlow to 50/ cmm. After 4 days of complete radiological and biological (Improved RFT, LFT), She had one episode of fever. Adequate measure were reassessed including sepsis marker and blood culture. Tachypnoea worstened in 6 to 8 hours with new infiltrates on chest x ray. Her elective intubation produced massive bleeding through ETT (Diffuse alveolar hemorrhage).

With all supportive measures again, she died on day 7 of admission ( 6 hours after second intubation)

Diagnosis- Macrophage Activation Syndrome (MAS) in case of vasculitis precipitated by acute viral infection


MAS is a severe systemic inflammatory reaction characterized by (uncontrolled) activation and proliferation of T cells and macrophages, with multiorgan infiltration and multiorgan dysfunction. Active haemophagocytosis by normal appearing macrophages is the pathognomonic feature of MAS. Though initially described  and thought typical of systemic onset juvenile idiopathic arthritis (So JIA) (it still remains the most common cause of MAS), it is now recognized in other rheumatic diseases in pediatric as well as in adult patients the fact that MAS is not uncommon, but also the fact that it is often not suspected clinically. This results in high mortality.

The characteristic immune abnormality of MAS is excessive (uncontrolled) proliferation of T cells and macrophages, along with overproduction of cytokines by these cells. The background immune abnormality is characterized by impaired cytotoxic function of NK cells and CD8 +ve T cells. It is postulated that this permits persistence of infecting organisms, resulting in persistent antigen driven T cell stimulation. Additionally NK cells are now recognized to play an immunoregulatory role also. Its impairment could permit T cell over activation.


Treatment of MAS is mainly supportive. More specifically underlying disease has to be treated. Treatment includes appropriate antibiotics and chemotherapeutic agents, corticosteroids, and immunosuppressive such as cyclosporin, cyclophosphomide, and IV immunoglobulin.Two types of agents are used.

  1. i) To interrupt the function of activated macrophages and histiocytes. These are etoposide, steroid, and high dose IV immunoglobulin
  2. ii) To interrupt the function of activated lymphocytes (T cells) – These are steroids,cyclosporin, and antithymocyte globulin. Since TNF-αlevels are elevated in MAS anti TNF-α agents have been used to achieve quick symptomatic relief. A commonly followed protocol consists of corticosteroids and etoposide with or without cyclosporin A.

In MAS corticosteroid treatment (high dose oral or methyl prednisolone pulses) is usually effective. Cyclosporin A,Indications for these would be uncontrolled fever, progressive pancytopenia, DIC, and impending organ failure.


MAS: Macrophage Activation Syndrome

ISCCM: Indian Society of Critical Care Medicine

SLED: Slow Low Efficienly Dialysis

ETT: Endo Tracheal Tube



1).Macrophage activation syndrome: JAPI Editorial: Dr.V.R.Joshi: Vol 55, March 2007

2)  J Assoc Physicians India, 2007; 55:185-7

Pinto L, Kagalwala F, Singh S, Balakrishna C, Prabhu SV, Khodaiji

  1. Macrophages activation syndrome: Experience from a tertiary

referral center.

3) Grom AA. Macrophage activation syndrome and reactive

hemophagocytic lymphocytosis: the same entities?

Curr Opin Rheumatol 2003; 15:587-90

4) Rituximab therapy in refractory macrophage activation syndrome secondary to systemic lupus erythematosus Lupus. 2013 Dec; 22(14):1544-6. doi: 10.1177/0961203313504634. Epub 2013 Sep 6.


Dr. Ajit Kulkarni

Consultant-Chest Disease, Interventional Pulmonology,

Critical Care Medicine


WITH protocolised treatment, Pulmonary tuberculosis is curable disease and sputum conversion with complete clearance on chest X ray / HRCT lung is achieved.

But We may find some sequlae like fibrosis, bronchiectasis & bronchial stenosis which makes patient permanently symptomatic even though the disease is cured.

We also get MDR TB, Endo bronchial TB as a consequence of inadequate treatment.

We use bronchoscopy diagnostically for BAL (Broncho Alveolar Lavage) for TB culture and mediastinal hilar Limphonode Biopsy (TBNA) for MDRV sampling. We also use bronchoscopy at the end of treatment scheduled for any scar malignancy. Post tubercular bronchiactasis is a seat for Aspergillosis which can be diagnosed by bronchoscopy.

We get bronchial stenosis which can be easily dealt with bronchoscopic balloon dilatation or electrocourty and dilatation to releave the symptoms.






When to ask for bronchoscopy in TB.

  1. Suspected MDR TB for BAL.
  2. Persistent wheeze or persistent cough.
  3. Symptomatically improved but partial recovery on chest X ray.
  4. Lung collapse / lung fibrosis.
  5. Total lung collapse
  6. Bronchiactasis on CT scan
  7. Bronchial or tracheal stenosis of balloon dilatation.      


Bronchoscopic management of benign bronchial stenosis by electrocautary and balloon dilatation: M Garg, Pratibha Gogia et. Al chest disease allie science 2012: 54:41-43.

Known Ys, Kim H, Kang KW, Such CY, Chung MP. the role of ballooning in patient with post tuberculosis bronchial stenosis. Tuberc Respir Dis 2009; 66:431-6.

N.Agrawal, D. Gupta, K.Joshi & S.K. Jindal “Endobronchial Involvement in Tuberculosis a report of 24 cases diagnosed by flexible bronchoscopy” journalof bronchology, vol 6, no 4, pp, 247 – 250 1999.

Wu, CY, Hu Hy, Pu CY et al: Pulmonary tuberculosis increases the risk of lung cancer: a population – based cohort study. cancer 2011, 117:618 – 24

Dr. Ajit Kulkarni

Consultant-Chest Disease, Interventional Pulmonology,

Critical Care Medicine

50 years Obese male was shifted to me from physician with history of progressive breathlessness of 2 days duration. It started with acute central chest pain with swatting following vomiting sensation. All cardiological work up was negative. He developed right pleural effusion on chest x ray and hence referred.

On arrival he had disproportionately severe breathlessness and tachycardia. Clinically and X Ray wise had right moderative severe pleural effusion. Diagnostic needle tap was done and fluid showed very high amylase level and was diagnostic. Immediate HRCT Lung with oral contrast withright lateral position CT Chest proved spontaneous esophageal rupture (Boer haave Syndrome), immediate ICD insertion was done to drain 2 liter of hemorrhagic fluid to releave his symptoms.

With due risk consent, he was subjected for repair of esophageal rupture by trans thoracic approach. He needed ventilator for 3 days and then NIV for next 10 days. His antibiotic policy was determined by culture report. After protracted course of 1 month, he was discharged home with recovery


Esophageal Rupture is a rupture of esophageal wall. 60% are iatrogenic usually due to endoscopy or surgery in contrast spontaneous rupture (Boerhaave Syndrome) accounts from 10% of cases which occult due to vomiting. It is full thickness tear due to sudden increase in esophageal pressure with relatively negative intrathoracic pressure caused by straining or vomiting.

It is uncommon diagnosis unless suspected by physician. There are no pathagnomic sign and symptoms. Prompt diagnosis with CT Scan, pleural fluid amylase level water soluble contrast esophagram (Gastro griffin) in lateral position can save the patient. If no help by a prompt surgery the mortality is 100%.


Esophageal Rupture & tear in emergency medicine clinical presentation: medscape: updated: December 2015.

Spontaneous Esophageal Rupture as the underlying cause of pneumothorax: early recognition is crucial: J of thoracic disease, 2014 December 6/12:1655 – 1658.

Bemard AW Ben-David K, Print T. Delayed presentation of thoracic esophageal Perforation after blunt trauma. J Emerg Med. 2008 Jan. 34 (1: 49:53 (Mediline)

Sinha R. Naclerio’s V sign. Radiology. 2007 Oct. 245(1): 296-7 (Mediline)

Altorjay A. Kiss J. Voros A, Bohak A. Nonoperative management of esophageal perforation. Is it justified? Ann Surg. 1997 Apr. 225(4): 415-21 (Mediline)

Dr. Ajit Kulkarni

Consultant-Chest Disease, Interventional Pulmonology,

Critical Care Medicine


25 years old female presented with history of Occasional Haemoptysis. She had vague chest pain. There were no systemic complaints like Fever or weight loss.Chest X Ray was unremarkable. Bronchoscopic examination showed tuft of hairs coming out of left upper lobe bronchus. There was no inflammation or mass or obstruction. CT scan chest revealed Hypodence Heterogeneous Lesion in anterior mediastinum with bronchial communication. She is subjected for surgical repair.12

Diagnosis: – Mediastinal Germ Cell Tumour with Bronchial Fistula.


Mediastinum Germ Cell Tumors, though rare, are well described in medical literature.

They are congenital Tumors containing derivatives of all germs layers.

Above 2/3 of benign teratomas are asymptomatic and are accidentally detected. They rarely rupture in to an adjacent structure, Such as plural cavity and pericardia cavity. However it is rare to have ruptured in to Tracheo – Bronchia tree as in our case.


 Mediastanal Dermoid with Bronchia Fistula.Vikas Suchdeva , Kavita Chavala(Ind. J. Thorac. Cardiovasc. Surg; 2007; 23.267 – 268)

Hiraiwa T; Hayshi T, Kaneda M, et al. Rupture of a benign mediastinal teratoma in to the right lural cavity. Ann Thorac Surg. 1991; 51; 110-12.

Biswas B. Mediastinal dermoid Presenting as a supra sterna fleshy mass. In J Thora cardiovasc surg 2006; 22:148 – 49.

Dr. Ajit Kulkarni

Consultant-Chest Disease, Interventional Pulmonology,

Critical Care Medicine


70 years female got admitted as an emergency admission with history of progressive worstning of respiratory distress of few days duration. She was received in emergency room in a drowsy state with GCS 6-7/15.

Her ABG showed Hypercarbic respiratory acidosis. She was immediately intubuted and ventilated.  She improved neurologically in 24 hours however, extubationtrial failed as she becomes drowse on T piece. Her MRI brain showed right Pontine Bleed with Cavernoma. CT chest shows evidence of COPD. She underwent Tracheostomy for long term ventilation and managed on invasive ventilator in ward and then in home.




Patient and relatives are taught about Tracheostomy,ventilatory care and possible accident with home ventilation.


1)Respiratory failure is the syndrome in which, system fails in one or both of its gases exchange.
2)Broadly Hypoxic failure is Type I and a Hypecarbic failure is Type II failure. Type II failure is charactoris by high PaCo2 (> 50)
3)PaCo2 is determined by level of alveolar ventilation. A decrease in alveolar ventilation can result from CNS depression like drugs, Neuro muscular disease primary brain stem disease and also COPD.
4)Type II failure has significant mortality in ICU especially Neurological Disease.
5)Long term ventilation is required quiet often and all its associated complication need to be discussed with relatives.

Dr. Ajit Kulkarni

Consultant-Chest Disease, Interventional Pulmonology,

Critical Care Medicine


A year back , 56 years male, was shifted to me by critical care Ambulance with NIV Ventilatory support for progressive Respiratory Distress. He had evidence of sepsis with hepatic Encephalopathy. His all workup including BAL was done and came positive for AFB- Tubercular Pneumonia. With Anti TB drugs and supports, He improved, sepsis disappeared and Liver functions improved as well. He continued anti TB treatment for 9 months and put on weight by 15 kg.

His x ray showed Right Upper Zone fibrosis. To discontinue his anti TB drugs I decided to Bronchoscopy & send BAL for AFB.

Surprisingly he showed Cauliflower growth in right main bronchus obstructing upper lobe bronchus. Histopath examination revealed poorly differentiated Squamous cell carcinoma.

Discussion: Lung cancer and pulmonary tuberculosis (TB) are two major public health problem associated with significant morbidity and mortality. The co-existence of TB and cancer has attracted attention for several years and has remained controversial. The association of TB & cancer is intriguing and diverse. Simultaneous occurrence of both TB and cancer in the same organ cause a diagnostic dilemma. Inflammation and scarring due to chronic TB result in metaplasia, dysplasia and cancer. On the other hand reactivation of latent TB in patients with cancer can occur because of immunosuppression due to malnutrition, aggressive chemotherapy and immunomodulatory therapy. The association between TB & cancer can occur in several ways. The possible association are:-

1)    A chance coincidence without any apparent relation
2)    Metastatic carcinoma developing in an old TB lesion.
3)    Secondary infection of cancer with Tb
4)    Chronic progressive tubercle in which a carcinoma develops
5)    Simultaneous development of both TB and cancer.

Experimental work in mice intended to prove the casual relationship between TB and cancer has shown that chronic TB infection can result in a multistep transformation of cell resulting in dysplasia and malignant squamous cell carcinoma by accumulation of genome alteration and effect of growth factors. Mycobacterium tuberculosis infected macrophages express high level of inducible nitric oxide synthase, resulting in the production of reactive nitrogen and oxygen species (ROS) leading to DNA damage. Activation of transcription factor, nuclear factor E2 related factor by oxidative stress, directly induced squamous cell metaplasia.·         In a population based cohort study in 5,657 TB patients and 23,485 age and qender – matched controls that were followed – up for 12 years showed  that the incidence of lung cancer was significantly higher in patients with pulmonary TB compared with controls with incident risk ratio (IRR) of 1.76. Cox proportional hazard model reveled pulmonary TB infection To be independent risk factors for lung cancer and concluded that pulmonary TB was associated with an increased risk of lung cancer.

·         In another cohort study conducted in 716,812 subjects including 4,480 patients with newly diagnosed TB who were followed – up for 7 years, incidence of lung cancer was found to be 11 fold higher in patients with Tb with a HR of 4.37 for TB cohort. The authors concluded that the there was an increased risk of lung carcinoma in patient with pulmonary TB.


1)Cancer and tuberculosis : review article : Journal , Indian Acadamy of Clinical Medicine2012;13(2):142-4
2)Wu, CY, Hu Hy, Pu CY et al: Pulmonary tuberculosis increases the risk of lung cancer: a population – based cohort study. cancer 2011, 117:618 – 24
3) Yu Yh, Liao CC, Hsu WH et al : Increased lung cancer risk among patients with pulmonary tuberculosis : a population cohort study J Thorac Oncol 2011: 6:32 -7

Dr. Ajit Kulkarni

Consultant-Chest Disease, Interventional Pulmonology,

Critical Care Medicine


A patient had presented to our hospital with the history of passing blood in the urine since last few months. He was operated in a private nursing home in Kolhapur for trans-urethral resection of prostate (TURP) surgery and was told to be suffering from prostate cancer. But his problem persisted. Another ultrasound scan (USG) done after a month shown a large tumour in the urinary bladder which was almost involving all the layers of urinary bladder and prostate also (T4).

He was operated at Aster Aadhar Hospital by team of two doctors (Dr Basavraj Kadalage – OncoSurgeon and Dr Amol Mutkekar – Urologist) for Radical Cysto-prostatectomy and ileal conduit urinary diversion. In this surgery, his entire urinary bladder and prostate gland was removed and a segment of ileum (small intestine) was interposed between ureters and abdominal wall so as to bring urine directly outside in a urine bag.

Surgery lasted for almost 9 hours and went well. Patient recovered without any complications and was discharged on 10th day post operatively. It’s been more than 8 months since surgery and the patient is doing well without disease recurrence and is on regular follow ups.

Dr. Basavraj Kadalage

Onco Surgeon


40 years lady admitted to our ICU with history of progressive breathlessness of two days duration.She had flu like symptoms for five to six days prior to this episode. She had bilateral extensive viral interstitial pneumonia. She was in TYPE I respiratory failure.Treated with NIV, NIV in prone position, oxygen augmentation and fluids, ceftriaxone, doxy and paracetamol. She remained critical and hypoxic for almost one month and progressively started improving. Sent home with NIV, oxygen and respiratory physiotherapy and supportive treatment. She continued this management in home for two months and gradually improved. At the end of two months her X-Ray is normal, blood gases are normal and 6MWD test improved substantially.


  1. Acute viral pneumonia with ARDS/interstitial pneumonia is quite common with disastrous outcome.
  2. They have prolonged protracted course.
  3. Need NIV/Intubation and ventilation for long time.
  4. They require domiciliary support of oxygen/NIV for couple of months, if they are hypoxic or have poor 6MWD on discharge.
  5. Prone NIV support is worth trying.
  6. Steroids have controversial role and we have not used them in these cases.

Before                                                   After

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Dr. Ajit Kulkarni

Consultant-Chest Disease, Interventional Pulmonology

Critical Care Medicine