Ultrasound Images and text by Genevieve Carbonatto
A 60 year old man presented to ED with a one day history of severe SOB on the background of a 2 month history of increasing SOB. He was so breathless that it was an effort to walk 3 to 4 metres. He had recently returned from a 2 year stay in Vietnam. No fevers or weight loss, no weight loss. An outpatient Chest Xray showed widespread reticular nodular infiltration in both lungs with an increased density in the LUL
Saturations: 95% on room air BP: 113 /73 HR: 100 RR: 28 Bloods:
This was his Xray on arrival to our Emergency Department
The Xray shows course interstitial infiltrates throughout the lungs with early alveolar confluence in the right lower lobe and apical pleural thickening on the left
At this stage TB or a metastatic process were high on the list as differential diagnoses and a CT was ordered
The CT showes multifocal nodular opacities and consolidation with central cavitation, interlobular and intralobular septal thickening and complete left lower lobe collapse
The most likely diagnosis was TB and he was to go to the ward to start anti mycobacterium treatment.
All done and dusted ……..
No – actually prior to going up to the ward he had a lung US and ECHO performed by the Emergency Physician
This is his lung ultrasound
There are clearly more than 3 B lines emanating from the pleural line between the 2 rib spaces. The B lines are wide and efface A lines. These B lines were widespread over his chest anteriorly. The costophrenic angles showed small pleural effusions as seen below
The differentials now included not only an interstital lung disease but also the possibility of pulmonary oedema or ARDS
An ECHO was performed. This is his PLAX view
The LV is clearly dilated and poorly contracting. Note the patchy appearance of the basal to mid LV inferolateral wall. There is a linear echogenic portion and then a more hypoechoic area at the base of the posterior mitral valve leaflet, (PMVL). This appearance should not be confused with a pericardial effusion. It is within the wall. Look at the motion of the atrioventricular groove. Compare this with the MRI comments.
His PSAX shows the poorly contracting LV. Again note the patchy appearance of the basal to mid LV inferolateral wall.
His ejection fraction using M mode in the PSAX was 31% and his LVOT VTI 9.01 cm confirming poor LVOT stroke volume, (SV). [LVOT SV x Heart rate] / 1000 = Cardiac output. If there is respiratory variation on PW Doppler trace of the LVOT, measure a minimum of two traces and average them (if time permits) or do after the study for a more accurate result. Normal LVOT vti = 17cm – 24cm. An LVOT of 9.0cm is obviously reduced.
This is his 4 chamber view. Again, the left ventricle is seen to be dilated and poorly contracting, the RV and RA on the other hand are of normal size when eyeballed.
It was clear therefore that this man not only had an underlying pulmonary disease, most likely TB but also a cardiomyopathy.
His acidfast bacilli on stain and Mtb were positive
His MRI below confirmed a patchy mid wall delayed enhancement in the basal to mid inferolateral wall consistent with an inflammatory process
How common is TB cardiomyopathy and does treatment improve outcome?
TB cardiomyopathy is rare.
It is thought to affect 1-2% of patients who have TB and mainly affects the pericardium and very rarely the myocardium or valves. TB is traditionally thought to spare the heart, the thyroid, the pancreas and skeletal muscle.
The myocardium can be affected in 3 ways: direct extension, retrograde lymphatic drainage from mediastinal nodes, direct spread from TB pericarditis. Endomyocardial biopsy confirms the diagnosis, but MRI is now used more frequently
Because of it’s relative rarity coupled by it’s insidious onset, TB myocarditis is more often diagnosed at postmortem. In the systematic review “Patterns and clinical manifestations of tuberculous myocarditis: a systematic review of cases” isolated cases of TB myocarditis without involvement of any other organs was found in only 25% of all reviewed cases. The review also concluded that anti-tuberculous drugs were effective in TB myocarditis by improving the clinical picture but did not reduce mortality due to sudden death.
It is worthwhile thinking of both respiratory and cardiac causes of shortness of breath (SOB) in the patient with TB. Point of Care ultrasound is an excellent rapid way of identifying an underlying cardiac problem.
- BMC Infec Dis 2005; 5: 29.Tuberculous dilated cardiomyopathy: an under-recognized entity?
Ritesh Agarwal,corresponding author1 Puneet Malhotra,1 Anshu Awasthi,2 Nandita Kakkar,2 and Dheeraj Gupta1
- Journal of Clinical and Diagnostic Research. 2011 June, Vol-5(3): 440-442 Cardiac Involvement in Patients with Pulmonary Tuberculosis; Rajesh S, Sricharan K.N, Jayaprakash K, Francis N P Monteiro
- Pan Afr Med J 2015; 21: 118.Patterns and clinical manifestations of tuberculous myocarditis: a systematic review of cases
Brian Nyasani Michira,1,& Faraj Omar Alkizim,1,2 and Duncan Mwangangi Matheka1,2