ABSTRACT
Horner syndrome is characterized by miosis, partial blepharoptosis and anhidrosis on the affected side of the face. This syndrome develops when the oculosympathetic nerve pathways to the eye and face are interrupted by various causes such as tumor in the brain, intrathoracic region or neck, surgery, drugs, trauma, carotid artery dissection, and others. It is referred to as painful Horner syndrome when Horner syndrome is accompanied by hemifacial pain. Pain is probably related to trigeminal nerve injury. Horner syndrome is a rare complication of thyroidectomy. Here, we report the case of a patient who experienced ipsilateral painful Horner syndrome after total thyroidectomy and unilateral neck dissection for thyroid cancer.
Subject(s)
Humans , Blepharoptosis , Brain , Carotid Artery Injuries , Horner Syndrome , Hypohidrosis , Miosis , Neck , Neck Dissection , Thyroid Neoplasms , Thyroidectomy , Trigeminal Nerve InjuriesABSTRACT
BACKGROUND: Flecainide is an antiarrhythmic agent that is used primarily in the treatment of cardiac arrhythmias. Some evidences also suggest that flecainide can participate in alveolar fluid clearance and inflammatory responses. This experiment was aimed to evaluate the effects of flecainide on sepsis induced acute lung injury in a rat model. METHODS: Rats were treated with subcutaneous infusion of saline or flecainide (0.1 or 0.2 mg/kg/hr) by a mini-osmotic pump. Subcutaneous infusion was started 3 hours before and continued until 8 hours after intraperitoneal injection of saline or endotoxin. Animals were sacrificed for analyses of severity of acute lung injury with wet to dry (W/D) ratio and lung injury score (LIS) in lung and inflammatory responses with level of leukocyte, polymorphonuclear neutrophils (PMNs) and inteleukin-8 (IL-8) in bronchoalveolar lavages fluid (BALF). RESULTS: Flecainide markedly improved dose dependently sepsis induced acute lung injury as analysed by W/D ratio (from 2.24 ± 0.11 to 1.76 ± 0.09, p < 0.05) and LIS (from 3 to 1, p < 0.05), and inflammatory response as determined by leukocyte (from 443 ± 127 to 229 ± 95, p < 0.05), PMNs (from 41.43 ± 17.63 to 2.43 ± 2.61, p < 0.05) and IL-8 (from 95.00 ± 15.28 to 40.00 ± 10.21, p < 0.05) in BALF. CONCLUSIONS: Flecanide improve sepsis induced acute lung injury in rats by controlling inflammatory responses.
Subject(s)
Animals , Rats , Acute Lung Injury , Arrhythmias, Cardiac , Bronchoalveolar Lavage , Flecainide , Infusions, Subcutaneous , Injections, Intraperitoneal , Interleukin-8 , Leukocytes , Lung , Lung Injury , Models, Animal , Neutrophils , SepsisABSTRACT
BACKGROUND: Flecainide is an antiarrhythmic agent that is used primarily in the treatment of cardiac arrhythmias. Some evidences also suggest that flecainide can participate in alveolar fluid clearance and inflammatory responses. This experiment was aimed to evaluate the effects of flecainide on sepsis induced acute lung injury in a rat model. METHODS: Rats were treated with subcutaneous infusion of saline or flecainide (0.1 or 0.2 mg/kg/hr) by a mini-osmotic pump. Subcutaneous infusion was started 3 hours before and continued until 8 hours after intraperitoneal injection of saline or endotoxin. Animals were sacrificed for analyses of severity of acute lung injury with wet to dry (W/D) ratio and lung injury score (LIS) in lung and inflammatory responses with level of leukocyte, polymorphonuclear neutrophils (PMNs) and inteleukin-8 (IL-8) in bronchoalveolar lavages fluid (BALF). RESULTS: Flecainide markedly improved dose dependently sepsis induced acute lung injury as analysed by W/D ratio (from 2.24 ± 0.11 to 1.76 ± 0.09, p < 0.05) and LIS (from 3 to 1, p < 0.05), and inflammatory response as determined by leukocyte (from 443 ± 127 to 229 ± 95, p < 0.05), PMNs (from 41.43 ± 17.63 to 2.43 ± 2.61, p < 0.05) and IL-8 (from 95.00 ± 15.28 to 40.00 ± 10.21, p < 0.05) in BALF. CONCLUSIONS: Flecanide improve sepsis induced acute lung injury in rats by controlling inflammatory responses.