Inhaled corticosteroids are the preferred treatment for children, however these drugs can reduce the growth rate. Acute symptoms are treated with short-acting bronchodilators. Pneumothorax
Pneumothorax presents typically with pleuritic chest pain of acute onset and shortness of breath not improved with oxygen. Physical findings may include absent breath sounds on one side of the chest, jugular venous distension, and tracheal deviation. Pneumonia
The symptoms of pneumonia are fever, productive cough, shortness of breath, and pleuritic chest pain. Inspiratory crackles may be heard on exam. A chest x-ray can be useful to differentiate pneumonia from congestive heart failure. As the cause is usually a bacterial infection, antibiotics are typically used for treatment. Pulmonary embolism
Pulmonary embolism classically presents with an acute onset of shortness of breath. Other presenting symptoms include pleuritic chest pain, cough, hemoptysis, and fever. Risk factors include deep vein thrombosis, recent surgery, cancer, and previous thromboembolism. It must always be considered in those with acute onset of shortness of breath owing to its high risk of mortality. Diagnosis, however, may be difficult and Wells Score is often used to assess the clinical probability. Treatment, depending on severity of symptoms, typically starts with anticoagulants; the presence of ominous signs (low blood pressure) may warrant the use of thrombolytic drugs. Anemia
Anemia that develops gradually usually presents with exertional dyspnea, fatigue, weakness, and tachycardia. It may lead to heart failure. Anaemia is often a cause of dyspnea. Menstruation, particularly if excessive, can contribute to anaemia and to consequential dyspnea in women.
Because this syndrome can be acquired or occur at random and has spontaneous resolution, Brown hypothesized one major truth for this disorder — that the short tendon sheath was due to a complete separation, congenital paresis, of the ipsilateral (on the same side) inferior oblique muscle and secondary to a permanent shortening.After further research, he redefined the sheath syndrome into the following divisions: true sheath syndrome, which categorized only the cases that had a congenital short anterior sheath of the superior oblique tendon, and simulated sheath syndrome, which characterized all cases in which the clinical features of a sheath syndrome caused by something different other than a congenital short anterior sheath of the tendon. The clinical features of the two categories are correct but true sheath syndrome is always congenital. However, in 1970 it was discovered that a tight sheath tendon was not the cause of Browns Syndrome. The real cause was a tight or short superior oblique tendon; studies have confirmed this and have labeled the tendon inelastic. Causes
Browns syndrome can be divided in two categories based on the restriction of movement on the eye itself and how it affects the eye excluding the movement:
Congenital (present at birth) Browns syndrome results from structural anomalies other than a short tendon sheath but other fibrous adhesions may be present around the trochlear area. Acquired cases arise from trauma, surgery, sinusitis and inflammation of the superior oblique tendon sheath in rheumatoid arthritis.