A70-18 The Lung Masks the Heart: Type II Respiratory Failure in A Post-Tubercular Patient With Dextrocardia

Introduction Post-tuberculosis lung disease (PTLD) represents a significant problem in regions with a high prevalence of tuberculosis. Persistent pulmonary changes, such as fibrosis, bronchiectasis, and volume depletion after successful tuberculosis treatment, can lead to deterioration of respiratory function and repeated hospitalizations. These sequelae can complicate the diagnosis and treatment of coexisting abnormalities, causing obstructive and restrictive changes that increase type II respiratory failure risk. Case A 69-year-old female with a history of post-tubercular fibrosis and baseline dyspnea grade 4 as per the modified Medical Research Council (mMRC), presented with complaints of worsening shortness of breath, pedal edema, and altered mentation for one day. The patient denied a history of smoking/alcohol use.On examination, vital signs: blood pressure of 90/60 mm Hg, pulse: 60 beats per minute, respiratory rate: 36 breaths per minute, temperature: 100 °F, and an oxygen saturation (Sp02) of 70% on room air. The patient was drowsy (GCS 6/15) and was placed on 5L O2 supplementation with improvement in SpO2 of 92%, jugular venous distension was also noted. Auscultation of the lungs revealed decreased vocal resonance with decreased breath sounds over the right upper lobe and left-sided crepitations. The apex beat and heart sounds were prominent on the right hemithorax. Investigations revealed worsening renal function (urea 124 → 211 mg/dL, creatinine 2.27 → 6.57 mg/dL. D-dimer was elevated at 8947 ng/mL, and arterial blood gases showed severe respiratory acidosis (pH 7.066, pCO2 132.1, PO2 134, HCO3 37.9) on admission, with partial improvement by the 8th day. Chest X-ray demonstrated right sided tracheal deviation, fibrocystic post-tubercular changes, and an obscured cardiac shadow. ECG revealed incidental finding of dextrocardia, confirmed by reversing the precordial leads. The patient was diagnosed with type II respiratory failure 2° to post-tuberculosis fibrosis and dextrocardia. Treatment included broad-spectrum antibiotics, diuretics, steroids, anticoagulation, and BIPAP (IPAP 24, EPAP 8). Discussion PTLD is characterized by a spectrum of changes, including fibrosis, bronchiectasis, and cavitation [1] They may obscure the identification of coexisting anomalies. These changes persist which affect the quality of life. Complications of TB after treatment can be often misinterpreted, therefore, it is essential to recognize and understand the radiologic manifestations and thoracic sequelae [2], to guide appropriate ventilatory support. Learning point In patients with prior pulmonary tuberculosis, extensive fibrotic distortion can mask underlying congenital anomalies as in our case. Comprehensive evaluation is crucial for prompt and appropriate management.