Phrenic nerve palsy in children associated with confirmed intrathoracic tuberculosis: diagnosis and clinical course.

In this descriptive retrospective cases series of eight cases phrenic nerve palsy in children caused by tuberculosis lymph gland infiltration of the phrenic nerve. The lymph gland enlargement was in all cases caused by culture confirmed Mycobacterium tuberculosis. The phrenic nerve palsy was on the left side in all eight cases with the presenting feature a raised diaphragm on chest radiography that was accompanied by consolidation of the left upper lobe (88%) The diagnosis of phrenic nerve palsy was confirmed by fluoroscopy of the chest. On computer tomography the outstanding features were left sided hilar and paratracheal lymph gland enlargement with displacement of the mediastinum to the right. Mediastinal displacement lead to anterior displacement of the descending aorta, which further compressed the left main bronchus. Two children had accompanying respiratory failure requiring assisted ventilation and in two additional cases the airway compression was so severe that glandular enucleation of the enlarged glands was indicated. Of the eight children five remained symptomatic after completion of TB treatment to which steroids were added for the initial month. Diaphragmatic plication was indicated in all five cases. On clinical follow-up two children had repeated respiratory tract infections secondary to underlying lung damage while the other six remained asymptomatic.

Is neuroborreliosis a medical emergency?

Although Lyme disease affects the nervous system in many ways (collectively known as neuroborreliosis), only rarely does it present as a medical emergency. In extreme cases, it may cause (1) encephalitis, (2) a rapidly progressive peripheral neuropathy, or (3) a painful truncal radiculopathy that may be confused with a severe visceral process. Knowing when to consider this spirochetosis in the differential diagnosis requires an understanding of its true clinical spectrum, and of an appropriate diagnostic and therapeutic approach.

[Role of nitric oxide in diaphragmatic dysfunction genesis during sepsis in rats]. / Rôle du monoxyde d'azote (NO) dans la genèse de la dysfonction diaphragmatique au cours du sepsis chez le rat.

Nitric oxide (NO) is a vasodilator agent that is cytotoxic and negatively inotropic in the heart. More recently, it has been shown that during sepsis there is a high amount of NO production by a NO synthase (NOS) that is inducible by cytokines. The aim of this study was to investigate the role of NO in the genesis of diaphragmatic dysfunction during sepsis. Rats were inoculated i.p. injection with 10 mg/kg of Escherichia coil endotoxin (E animals) or saline (C animals). Six hours after endotoxin or saline inoculation, diaphragmatic force and muscularc GMP (Cyclic guanosine monophosphate) were assessed by in vitro force frequency curves and ELISA method, respectively. As compared to C animals, E animals showed a significant decrease in diaphragmatic force for all the frequencies of stimulation (p < 0.01). This reduction was associated with a significant increase in muscular cGMP. Inhibition of NO synthesis in E animals with either dexamethasone (4 mg/kg IV, 45 min before endotoxin or saline) or NG-monomethyl-L-arginine (L-NMMA, 8 mg/kg IV, 90 min after endotoxin or saline) prevented the effects of endotoxin. However, no modification was seen with NG-monomethyl-D-arginine (D-NMMA), a molecule which does not inhibit NO synthesis. Administration of dexamethasone or L-NMMA in C animals did not induce any significant change in diaphragmatic force, and cGMP ratio. We conclude that NO has a contributive role in diaphragmatic dysfunction during Escherichia coli induced sepsis in rats.