In these cases, glucocorticoids, aerosolized epinephrine, or helium oxygen therapy may be considered as part of the management plan.Patients who are clinically stable with no need for supplemental oxygen after extraction may be discharged from the hospital the same day as the procedure. Routine imaging such as a follow-up chest x-ray are not needed unless symptoms persist or worsen, or if the patient had imaging abnormalities previously to verify return to normal. Most children are discharged within 24 hours of the procedure. Complications
Many complications can develop if a foreign body remains in the airway. There are also complications that may occur after removal of the object depending on the timeline of events. Cardiac arrest and death are possible complications if a sudden complete obstruction occurs and immediate medical care is not performed. The most common complication from a foreign body aspiration is a pulmonary infection, such as pneumonia or a lung abscess. This can be more difficult to overcome in the elderly population and lead to even further complications. Patients may develop inflammation of the airway walls from a foreign body remaining in the airway. Airway secretions can be retained behind the obstruction which creates an ideal environment for subsequent bacterial overgrowth. Hyperinflation of the airway distal to the obstruction can also occur if the foreign body is not removed.
However mice lacking both copies of ataxin 1 do not develop progressive neurological symptoms or show signs of atrophy, suggesting that toxicity of the mutated protein, not loss of function, is the main mechanism for SCA1 pathology. A comparison of mRNA  between ataxin null mice and mice with ataxin1154Q/+ shows that there are common changes in gene expression, including upregulation of genes known to be repressed by an ataxin 1/CIC complex. This suggest that, while not the primary mechanism, a loss of ataxin 1 function contributes to the pathogenesis of SCA1. While the ataxin 1/CIC complex losses some of its regulatory function with expanded ataxin 1, CIC knockout mice do not show degeneration, suggesting interactions between ataxin 1 and CIC mediate most of the toxic effects. Mutant ataxin-1 also known to alter the neural circuitry of the developing cerebellum, which may lead to later vulnerability of Purkinje cells and suggests the existence of non-cell autonomous toxicity.The various interactions of ataxin 1 lead to many possible factors that can exasperate or moderate toxicity of its mutant form. Wild type ataxin 1 is quickly degraded in the cytoplasm, but can be stabilized by phosphorylation and 14-3-3 binding as needed by the cell. SCA1 positive mice haplodeficient in 14-3-3ε+/- were shown not to exhibit cerebellar degeneration but still exhibited lethal bulbar degeneration, suggesting that cerebellar atrophy may be related to increased stability of the expanded ataxin 1 protein and that there may be different pathogenic mechanisms for different regions of the brain.