Steroids in cavernous sinus thrombosis

Chronic rhinosinusitis is an inflammatory condition of the paranasal sinuses that most often causes chronic sinonasal symptoms. In the United States, chronic rhinosinusitis has an estimated prevalence of 1% to 5%. It is a readily treatable disease that is responsible for direct and indirect health care expenses totaling billions of dollars every year in the United States. 1 , 2 Because the pathophysiology of chronic rhinosinusitis in children is distinct from that in adults, and the medical and surgical approach differs significantly between children and adults, 3 this review focuses on adult chronic rhinosinusitis.

In the treatment of a brain cavernous hemangioma, neurosurgery is usually the treatment chosen. [25] Research needs to be conducted on the efficacy of treatment with stereotactic radiation therapy , especially on the long-term. [26] However, radiotherapy is still being studied as a form of treatment if neurosurgery is too dangerous due the location of the cavernoma. Genetic researchers are still working on determining the cause of the illness and the mechanism behind blood vessel formation. [23] Clinical trials are being conducted to better assess when it is appropriate to treat a patient with this malformation and with what treatment method. [9] Additionally, long term studies are being conducted because there is no information related to the long-term outlook of patients with cavernoma. A registry exists known as The International Cavernous Angioma Patient Registry collects information from patients diagnosed with cavernoma in order to facilitate discovery of non-invasive treatments. [23]

The role of Botox? for acute sixth nerve palsy remains unsettled (Figure 3). It has been used to attempt to prevent or reduce the contracture of the antagonist medial rectus, and also to treat small postoperative deviations. The known occurrence of spontaneous recovery of some sixth nerve palsies clouds the interpretation of case-report studies. Reports sometimes include various etiologies, both traumatic and nontraumatic, lumped together. Hung reported a higher functional recovery rate in a retrospective study in 14 of 33 patients with acute complete traumatic sixth nerve palsies who were treated with Botox?. [15] Holmes reviewed the course of 84 patients with traumatic sixth nerve palsies, 22 of whom were treated with Botox? and the remainder treated conservatively. He found no difference in the outcome of the patients. [16] Biglan reported that 7 of 16 patients with sixth nerve palsy were controlled by Botox?, and that patients with long-standing or severe palsy did not get as positive a result as patients with more acute palsies or with better lateral rectus function. [17] In a study of nine children with brain neoplasms accompanied by sixth nerve palsies, treatment with Botox? was not felt to hasten recovery. [18] Eight patients with nontraumatic sixth nerve palsies were reported to have excellent results from Botox?, with seven having no diplopia in the long term. [19] Complications of Botox? included ptosis, induced hypertropia, subconjunctival hemorrhage, possible globe perforation, and failure to maintain an effect.

A patient developing sudden enlargement and firmness in a preexisting large hemangioma, with easy bruising and petechiae, should be suspected of having Kasabach-Merritt syndrome, a coagulopathy characterized by thrombocytopenia occurring in patients with large hemangiomas. Platelet trapping within the enlarging hemangioma may result in secondary disseminated intravascular coagulation. These patients require hospitalization and treatment with prednisone (2 to 4 mg per kg per day) or interferon alfa-2a (Roferon-A) in steroid-resistant patients. External compression bandages and transfusion of supportive blood products facilitate recovery. If hemorrhage is prevented, recovery is usually complete. 3

CST most commonly results from contiguous spread of infection from a nasal furuncle (50%), sphenoidal or ethmoidal sinuses (30%) and dental infections (10%). [3] Less common primary sites of infection include tonsils, soft palate, middle ear, or orbit ( orbital cellulitis ). The highly anastomotic venous system of the paranasal sinuses allows retrograde spread of infection to the cavernous sinus via the superior and inferior ophthalmic veins. It was previously thought that veins in the area were valveless and that this was the major cause of the retrograde spread, however, a recent study has found that the ophthalmic and facial veins are not valveless. [4]

Steroids in cavernous sinus thrombosis

steroids in cavernous sinus thrombosis

A patient developing sudden enlargement and firmness in a preexisting large hemangioma, with easy bruising and petechiae, should be suspected of having Kasabach-Merritt syndrome, a coagulopathy characterized by thrombocytopenia occurring in patients with large hemangiomas. Platelet trapping within the enlarging hemangioma may result in secondary disseminated intravascular coagulation. These patients require hospitalization and treatment with prednisone (2 to 4 mg per kg per day) or interferon alfa-2a (Roferon-A) in steroid-resistant patients. External compression bandages and transfusion of supportive blood products facilitate recovery. If hemorrhage is prevented, recovery is usually complete. 3

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