CRA54 AN UNUSUAL INTERSECTION: TUBERCULOSIS AND GUILLAIN-BARRE SYNDROME IN A COMPLEX CLINICAL PRESENTATION

Affida Ahmad,1 Am Basheri Alias1, Mimi Nashra Mohd Noh2, Shalini Bhaskar2, Aisya Natasya Musa1.
1 Respiratory Unit, Universiti Teknologi MARA (UiTM), Puncak Alam Selangor, Malaysia
2 Neurology Unit, Universiti Teknologi MARA (UiTM), Puncak Alam Selangor, Malaysia

Introduction:

Guillain-Barre Syndrome (GBS) manifests as an acute inflammatory polyradiculoneuropathy, typically arising from an immune-mediated response triggered by antecedent infections. This case report sheds light on an intriguing association between GBS and tuberculosis (TB), a relationship that remains relatively obscure despite emerging reports linking the two conditions.

Case Report:

A 63-year-old man with poorly controlled Type 2 diabetes mellitus, hypertension and ischemic heart disease presented with worsening left-sided chest pain persisting for a month, He also reported six-month history of constitutional symptoms and a cough following exposure to his wife, recently treated for TB. Upon admission, he was febrile (38.3OC), hypotensive (101/60 mmHg necessitating single inotropic support) with respiratory rate of 20 breaths/minute, and an oxygen saturation of 95% on room air. Clinical examination revealed dullness to percussion, corroborated by thoracic ultrasound and chest X-ray findings indicative of moderate left-sided pleural effusion. Initial investigations revealed leukocytosis, elevated C-reactive protein and a pleural effusion exudative profile. During his hospitalization, the patient developed hypoxia attributed to worsening pleural effusion and bilateral subsegmental pulmonary embolism, necessitating pleural drainage and anticoagulation. Empirical initiation of antibiotic and anti-TB therapy was undertaken. On the third day of admission, the patient reported progressive weakness in his lower limbs, subsequently extending to symmetric upper limb weakness, with lower limb power declining from 4/5 to 2/5, accompanied by absent reflexes. Refusal for lumbar puncture was noted. Nerve conduction studies confirmed acute inflammatory demyelinating polyneuropathy (AIDP) consistent with GBS. Concomitantly, sputum Mycobacterium tuberculosis culture and sensitivity yielded positive results for TB sensitive to first-line anti-TB agents, whereas blood and pleural fluid cultures remained negative. Following five plasma exchange sessions, his limb power improved from 2/5 to 5/5 with persistent areflexia.

Discussion:

This case underscores the need to consider TB in GBS management despite its uncommon association, emphasizing timely intervention for optimal outcomes.