Artritis séptica neumocócica de rodilla como causa de enfermedad tromboembólica venosa / Venous Thromboembolic Disease due to septic pneumococcal arthritis of the knee

La artritis séptica neumocócica es una entidad poco frecuente en adultos. Se produce por una disemincación hematógena desde algún foco infeccioso. La afectación poliarticular es menos frecuente si bien es más frecuente que en otros patógenos causantes de artritis. Presentamos el caso de una paciente con artritis séptica neumocócica en la rodilla derecha secundaria a una neumonía, la compresión de la cual causó una trombosis venosa profunda (TVP) en la extremidad ipsilateral y un tromboembolismo pulmonar (AU)

Streptococcus pneumoniae induced septic arthritis is very rare in adults. It is produced by hematogenous spread from other infectious areas. Polyarthritis involvement is less frequent, although it is more frequent than in other arthritis causing pathogens. We report a clinical case of a woman with septic pneumococcal arthritis of the knee secondary to pneumonia, the compression of which caused deep venous thrombosis (DVT) in the ipsilateral limb and pulmonary thromboembolism (AU)

Clinical trial: a randomized controlled study on prevention of variceal rebleeding comparing nadolol + ligation vs. hepatic venous pressure gradient-guided pharmacological therapy.

BACKGROUND: Hepatic venous pressure gradient (HVPG) monitoring of therapy to prevent variceal rebleeding provides strong prognostic information. Treatment of nonresponders to beta-blockers +/- nitrates has not been clarified. AIM: To assess the value of HVPG-guided therapy using nadolol + prazosin in nonresponders to nadolol + isosorbide-5-mononitrate (ISMN) compared with a control group treated with nadolol + ligation. METHODS: Cirrhotic patients with variceal bleeding were randomized to HVPG-guided therapy (n = 30) or nadolol + ligation (n = 29). A Baseline haemodynamic study was performed and repeated within 1 month. In the guided-therapy group, nonresponders to nadolol + ISMN received nadolol and carefully titrated prazosin and had a third haemodynamic study. RESULTS: Nadolol + prazosin decreased HVPG in nonresponders to nadolol + ISMN (P < 0.001). Finally, 74% of patients were responders in the guided-therapy group vs. 32% in the nadolol + ligation group (P < 0.01). The probability of rebleeding was lower in responders than in nonresponders in the guided therapy group (P < 0.01), but not in the nadolol + ligation group (P = 0.41). In all, 57% of nonresponders rebled in the guided-therapy group and 20% in the nadolol + ligation group (P = 0.05). The incidence of complications was similar. CONCLUSIONS: In patients treated to prevent variceal rebleeding, the association of nadolol and prazosin effectively rescued nonresponders to nadolol and ISMN, improving the haemodynamic response observed in controls receiving nadolol and endoscopic variceal ligation. Our results also suggest that ligation may rescue nonresponders.