Nasal obstruction (NO) is defined as the subjective perception of discomfort or difficulty in the passage of air through the nostrils. It is a common reason for consultation in primary and specialized care and may affect up to 30%-40% of the population. It affects quality of life (especially sleep) and lowers work efficiency. The aim of this document is to agree on how to treat NO, establish a methodology for evaluating and diagnosing it, and define an individualized approach to its treatment. NO can be unilateral or bilateral, intermittent or persistent and may be caused by local or systemic factors, which may be anatomical, inflammatory, neurological, hormonal, functional, environmental, or pharmacological in origin. Directed study of the medical history and physical examination are key for diagnosing the specific cause. NO may be evaluated using subjective assessment tools (visual analog scale, symptom score, standardized questionnaires) or by objective estimation (active anterior rhinomanometry, acoustic rhinometry, peak nasal inspiratory flow). Although there is little correlation between the results, they may be considered complementary and not exclusive. Assessing the impact on quality of life through questionnaires standardized according to the underlying disease is also advisable. NO is treated according to its cause. Treatment is fundamentally pharmacological (topical and/or systemic) when the etiology is inflammatory or functional. Surgery may be necessary when medical treatment fails to complement or improve medical treatment or when other therapeutic approaches are not possible. Combinations of surgical techniques and medical treatment may be necessary.

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Adverse reactions to nonsteroidal antiin¯ammatory drugs (NSAID) have been recognized for years. Such reactions include acute asthmatic attacks or perpetuation of ongoing asthma, initiation or perpetuation of chronic urticaria, and anaphylactic or anaphylactoid episodes (1). In this paper, we report the case of an infrequent NSAID adverse effect con®rmed by oral challenge test. This case illustrates indomethacin-and acetylsalicylic acid (ASA)-induced seizures. A 65-year-old man without a remarkable neurologic and atopic medical history had an episode of seizures about 15 min after ingestion of one Inacid 2 tablet (indomethacin 50 mg). He had taken no other medication. The man complained of abdominal pain and rapid onset of profuse sweating, loss of consciousness, tonic extension of the arms, and turned up eyes, without urinary incontinence. The symptoms resolved within 3±4 min without treatment, with slow return to complete lucidity: after seizure, the patient was confused, sleepy, and uncooperative for several minutes before full recovery. Results of physical examination were unremarkable, neurologic examination showed no abnormalities other than limited drowsiness. General analysis and kidney function were normal, as was computed tomography (CT) of brain, electroencephalogram (EEG), and Holter electrocardiogram. During the allergologic evaluation, the patient was orally challenged, after giving written, informed consent. A single, nonchewable, 50-mg indomethacin tablet (regularstrength Inacid) was used. The patient repeated the previous clinical features 10 min after the ingestion of the tablet. He had no other symptoms. We also performed oral challenge with ASA, and diclofenac, with good tolerance. The patient was followed up for 2 years, and during this time he received ASA on several occasions without dif®culty. After this period of time, he presented a new episode of seizures, similar to those previously described, 10 min after ingestion of 500 mg ASA. General and neurologic examination, general analysis, kidney function, brain CT, and EEG were again normal. After discussion with him about adverse reactions to NSAID, a new challenge was undertaken only with salicylate and isonixin, with tolerance. The patient did not have any symptoms during or after the challenge. We did not perform oral challenge with AAS and other NSAID because informed consent was not given by the patient. Many drugs are known to cause convulsions in many different circumstances. In order to focus on this problem properly, one must clearly distinguish between situations in which this adverse effect is observed at therapeutic dosages and conditions in which seizures are part of the clinical picture of poisoning (2). In this particular case, the seizures developed after standard dosage of the drugs, and they were not followed by other symptoms. These features indicate NSAID to be the trigger factor. Seizures have occasionally been reported during NSAID therapy: mefenamic acid (3), ibuprofen (4), and diclofenac (5) have been implicated. In ...