IntroductionTransvenous pacing is a relatively safe treatment with a low complication rate, but serious thromboembolic complications have been reported to occur in 0.6% to 3.5% of cases. Superior vena cava obstruction syndrome is generally an uncommon but serious complication occurring in <0.1% of patients. However, when it occurs it carries with it significant morbidity and mortality.Case presentationA 51-year-old lady with long history of DDD permanent pacemaker presented following a mechanical fall. She had no obvious injuries, and was hemodynamically stable. General examination revealed features suggestive of Superior vena caval obstruction which was later confirmed by imaging. She was treated with long term oral anticoagulation with good clinical improvement.ConclusionSuperior vena cava obstruction in patients with transvenous pacing leads, although rare, is a well recognized complication. With growing elderly population and increasing number of procedures performed, more and more people with permanent pacemaker are likely to be encountered in clinical practice. One should carefully look for thromboembolic complications during follow-up in patients with transvenous pacemaker leads, as it has implications for future management and carries significant morbidity and mortality.
A 71-year-old man was admitted with generalized tiredness, mild confusion and low-grade pyrexia following the fourth cycle of intravesical bacillus Calmette–Guérin instillation for the treatment of superficial bladder carcinoma. These symptoms were accompanied by some weight loss which was difficult to quantify. His past medical history included type 1 diabetes mellitus, chronic obstructive pulmonary disease and prostatic hyperplasia. He was a smoker and consumed a moderate amount of alcohol. Physical examination was unremarkable with the exception of confusion (abbreviated mental test score 7/10). Initial investigations showed low serum sodium of 122 mmol/litre with normal potassium, renal and thyroid functions. His liver functions were abnormal with aspartate transferase of 76 IU/litre and alkaline phosphatase 286 U/litre. Chest X-ray showed bilateral non-specific reticular changes suggestive of infection. Two sets of blood cultures showed no growth after 72 hours. Urine tests for legionella and pneumococcal antigen were negative. Computed tomography of the brain revealed deep white matter changes suggestive of small vessel disease. On further investigations urine osmolality was 546 mOsm/kg, serum osmolality 256 mOsm/kg, urine sodium 61 mmol/litre and the short Synacthen test was normal, confirming the diagnosis of syndrome of inappropriate antidiuretic hormone. After fluid restriction to 1 litre per day his sodium level started to improve slowly, but the patient's condition continued to deteriorate with ongoing low-grade pyrexia, confusion and lethargy. A repeat chest X-ray 5 days later (Figure 1) showed multiple small non-calcified nodules in both lungs raising the possibility of miliary tuberculosis. This was confirmed on high resolution computed tomography scan of the chest (Figure 2) as presence of bilateral diffuse miliary shadowing in keeping with a diagnosis of miliary tuberculosis. In view of his confusion, CSF examination was done to rule out CNS involvement, but this was normal. No endobronchial lesions were identified on bronchoscopy and bronchial washings were sent for analysis and cultures. The patient was started on anti-tuberculous treatment (isoniazid, rifampicin and ethambutol) as well as steroids and pyridoxine. Unfortunately, the patient suffered a cardiac arrest and died a week after starting the treatment. Cultures of bronchial lavage and CSF did not grow any mycobacterium. On post-mortem examination he was found to have multiple small whitish nodules in both lungs, with caseating granulomata, central areas of necrosis and multinucleated giant cells microscopically.
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