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This article has overviewed complications of rhinoplasty. Generally, these complications fall into two categories: aesthetic (that is, cosmetic sequelae that may require a revision rhinoplasty) and nonaesthetic. Of the nonaesthetic complications, infection has the widest span of severity. A localized Staphylococcus aureus abscess or Pseudomonas infection of the nose may occur postoperatively. Owing to the proximity of the nose to the cranium, a cavernous sinus thrombosis or basilar meningitis may result. Postoperative toxic-shock syndrome is a rare occurrence that surgeons should be aware of; most cases have occurred with the presence of nasal packing, but a case using only plastic nasal splints has been reported also. Bacteremia seems to be uncommon during rhinoplasty. Infection after rhinoplasty is generally much less frequent than one would expect from an operation in an unsterile field. Antibiotics are frequently utilized electively. Postoperative nasal-periorbital edema and ecchymosis are regarded as unavoidable but may be lessened significantly by postoperative head elevation and cold packs. The possibility of postoperative bleeding must be evaluated by the surgeon preoperatively. This sequela usually occurs either within 72 hours postoperatively or at around 10 days postoperatively. Many different causes exist for chronic postoperative nasal obstruction, from poorly supported nasal valves closing upon inspiration to an enhanced allergic rhinitis leading to chronic nasal mucosal edema. The latter may be treated by injection of steroid into the turbinates. Among aesthetic complications, supratip prominence, saddle deformity, and persistent hump are among the more commonly reported. Supratip prominence--"polly-beak"--can be caused by inadequate reduction of tip cartilaginous or soft-tissue elements, especially in relation to the reduction of the dorsum. An over-reduced dorsum will leave an otherwise normal nasal tip with a relative prominence. An accumulation of blood or a mucous cyst occurring under the skin of the tip will produce a prominence. Poor tip projection, tip ptosis, and alar collapse are the result of overreduction of tip elements. A dislocated alar cartilage can appear as an asymmetric nasal bossa. Saddle-nose deformity occurs after overaggressive bony and/or cartilaginous hump removal. Infractured nasal bones that subsequently drop into the piriform aperture can create a bony saddle. Persistent hump is due to inadequate reduction of a bony or cartilaginous hump. If the septal cartilage reduction is disproportionate to the bony septum reduction, the appearance of either a hump or a saddle is possible.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Postoperative sequelae and complications of rhinoplasty. 332 Aug 72

We identified two siblings with exercise-induced anaphylaxis who share the HLA haplotype A3-B8-DR3 with their atopic father. The index case, a 16-year-old female, noted initial episodes at age 13. Intense pruritus, urticaria, facial edema, choking sensation, nausea, hypothermia, and collapse followed vigorous running but not swimming, cycling, racquetball, solar exposure, or cold exposure. Neither antihistamine, antiserotonin, anticholinergic nor epinephrine therapy was entirely effective or protective; only modification of running prevented episodes. Three similar episodes were noted at age 15 years by a brother who, now age 25, relates a 4-year history of seasonal rhinitis and exercise-related urticaria without anaphylactoid reaction. The remainder of the family (father, 47; mother, 46; brother, 22 years) does not have exercise intolerance. The father has allergic rhinitis; his nephew suffers exercise-induced urticaria without collapse. HLA typing revealed the father to be A1-B8-DR3, A3-B8-DR3; the symptomatic daughter to be A3-B8-DR3, A30-B5-DR8; and the symptomatic son to be A3-B8-DR3, A30-B5-DR8. The asymptomatic mother was A30-B5-DR8, A2-B7-DR5 and the asymptomatic son A1-B8-DR3, A30-B5-DR8. We describe exercise-induced anaphylaxis in a unique familial setting, perhaps linked to the HLA haplotype A3-B8-DR3.
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PMID:Familial exercise-induced anaphylaxis. 347 Oct 98

Obstructive sleep apnea (OSA) is a common condition of childhood, and is associated with significant morbidity. Prevalence of the condition peaks during early childhood, due in part to adenoidal and tonsillar enlargement within a small pharyngeal space. The lymphoid tissues regress after 10 years of age, in the context of ongoing bony growth, and there is an associated fall in the prevalence of OSA. Obstruction of the nasopharynx by adenoidal enlargement promotes pharyngeal airway collapse during sleep, and the presence of large tonsils contributes to airway obstruction. Administration of systemic corticosteroids leads to a reduction in the size of lymphoid tissues due to anti-inflammatory and lympholytic effects. However, a short course of systemic prednisone has been demonstrated not to have a significant effect on adenoidal size or the severity of OSA, and adverse effects preclude the long-term use of this therapy. Intranasal corticosteroids are effective in relieving nasal obstruction in allergic rhinitis, and allergic sensitization is more prevalent among children who snore than among those who do not snore. Intranasal corticosteroids have also been demonstrated to reduce adenoidal size, independent of the individual's atopic status. There is preliminary evidence of an improvement in the severity of OSA in children treated with intranasal corticosteroids, but further studies are needed before such therapy can be routinely recommended. Prescribing clinicians should take into account the potential benefits to the patient, the age of the child, the presence of comorbidities such as allergic rhinitis, the agent used, and the dose and duration of treatment when considering such therapy.
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PMID:Obstructive sleep apnea in children: do intranasal corticosteroids help? 1472 53

Laryngomalacia is the most common cause of stridor in neonates and infants, where the soft cartilages and tissues surrounding the upper larynx collapse inward during respiration. On the other hand, acquired idiopathic laryngomalacia in adults is quite rare, but should be borne in mind for differential diagnosis of upper airway distress. Allergic factors may cause airway distress, but have not been highlighted previously as the background of laryngomalacia. In this report, we describe two patients with acquired idiopathic laryngomalacia with reference to allergic rhinitis and high serum levels of immunoglobulin E. The first patient was a 16-year-old female who presented with inspiratory stridor and dyspnea due to attachment between the epiglottis and bilateral arytenoids, and the second patient was an 18-year-old male who also presented with inspiratory stridor due to attachment between the epiglottis and posterior pharyngeal wall. The respiratory function of both patients was within the normal range but the inspiratory stridor interfered with daily life. Laryngomicrosurgery was performed in both patients using a CO2 laser to remove the arytenoid mucosa in the first patient, and to remove the tip of the epiglottis in the second. Both patients were followed up while receiving oral anti-allergic agents. Laser supraglottic laryngoplasty to remove the vibrating excess tissue was effective for resolving the symptoms. However, recurrence occurred three times in the first patient, and inferior turbinotomy to improve nasal respiration was useful for diminishing the symptoms.
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PMID:Acquired idiopathic laryngomalacia treated by laser supraglottic laryngoplasty. 2372 5

Anaphylaxis is an acute, severe, life-threatening multisystem allergic reaction resulting from the sudden systemic release of biochemical mediators and chemotactic substances. Release of both preformed granule-associated mediators and newly generated lipid-derived mediators contributes to the amplification and prolongation of anaphylaxis. Platelet-activating factor (PAF) is a potent phospholipid-derived mediator the central role of which has been well established in experimental models of both immune-mediated and non-immune mediated anaphylaxis. It is produced and secreted by several types of cells, including mast cells, monocytes, tissue macrophages, platelets, eosinophils, endothelial cells, and neutrophils. PAF is implicated in platelet aggregation and activation through release of vasoactive amines in the inflammatory response, resulting in increased vascular permeability, circulatory collapse, decreased cardiac output, and various other biological effects. PAF is rapidly hydrolyzed and degraded to an inactive metabolite, lysoPAF, by the enzyme PAF acetylhydrolase, the activity of which has shown to correlate inversely with PAF levels and predispose to severe anaphylaxis. In addition to its role in anaphylaxis, PAF has also been implicated as a mediator in both allergic and nonallergic inflammatory diseases, including allergic rhinitis, sepsis, atherosclerotic disease, and malignancy, in which PAF signaling has an established role. The therapeutic role of PAF antagonism has been investigated for several diseases, with variable results thus far. Further investigation of its role in pathology and therapeutic modulation is highly anticipated because of the pressing need for more selective and targeted therapy for the management of severe anaphylaxis.
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PMID:Platelets in the immune response: Revisiting platelet-activating factor in anaphylaxis. 2605 49

Agenesis of the right upper lobe of the lung is a very uncommon congenital anomaly and may be referred to chest clinics in adulthood for an incidental finding of abnormal chest radiograph. The presentations of chest radiograph may imitate many common situations such as right upper lobe collapse presenting as an ipsilateral shifting of the mediastinum or elevation of the right hemidiaphragm due to eventration or subdiaphragmatic lesions. A chest computed tomography is considered the most conclusive examination used to diagnose lung agenesis. Three-dimensional reconstructed images can be particularly helpful in delineating abnormalities of the bronchi and associated arterial and venous structures. We describe here a young woman with allergic rhinitis and bronchial asthma since her early childhood. She was referred to our clinic for an incidental finding of abnormal chest radiograph after a school health checkup. Right upper lobe atelectasis or intra-abdominal lesions were initially suspected. After a thorough image study, she was diagnosed as a case of agenesis of the right upper lobe. Our report emphasizes the importance that a high index of suspicion and adequate image investigation are necessary to diagnose congenital lung anomalies.
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PMID:Agenesis of right upper lobe of lung. 2609 Jan 10

Leukotriene receptor antagonists, which are generally considered safe with a few adverse drug reactions, are increasingly used in the treatment of various allergic diseases, including asthma and allergic rhinitis. Although a few anaphylactic reactions to montelukast have been reported worldwide, there is still a lack of reports about severe adverse drug reactions associated with pranlukast. Here, we report a case of severe hypersensitivity reaction associated with pranlukast. A 65-year-old woman developed anaphylactic shock that presented as generalized urticaria, angioedema, collapse, and loss of consciousness after receiving pranlukast. A positive response to oral challenge and skin prick testing with pranlukast was observed in the patient. In this case, it was demonstrated that pranlukast can induce anaphylaxis, possibly mediated by the IgE-dependent pathway.
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PMID:A Case of Pranlukast-Induced Anaphylactic Shock. 2692 38

We present a case of a 76 year-old, non-smoking Honduran female who was referred to our clinic for years of persistent dry cough. Cardiac evaluation was unremarkable. She denied symptoms of heartburn, allergic rhinitis, and there was no personal or family history of asthma. Her physical exam demonstrated wheezing over the right mid-posterior chest. Spirometry was within normal limits. CT-imaging of the chest demonstrated right middle lobe bronchus and lingular segmental bronchus narrowing with bibasilar atelectasis and mild interlobular septal thickening with prominent mediastinal adenopathy. Bronchoscopy showed diffuse airway hyperpigmentation, right middle lobe medial segmental bronchial stenosis and lingular segmental bronchial stenosis. Endobronchial ultrasound demonstrated enlarged mediastinal lymph nodes, and transbronchial needle aspirates revealed necrotic tissue with black anthracotic pigment. Cultures were negative. Post-procedurally, the patient revealed regular use of a wood stove in an enclosed, poorly-ventilated kitchen. Anthracosis is the black discoloration of bronchial mucosa due to deposition of carbon-based particles in the airway, usually related to chronic environmental exposures. It can eventually result in endobronchial and parenchymal fibrosis and is mostly seen in non-smokers. Burning biomass fuel from wood smoke is a risk factor in the developing world. Symptoms include cough, dyspnea, and wheezing. Spirometry will usually demonstrate obstruction. CT-based imaging can show intraluminal narrowing, predominantly affecting the right middle and right upper lobe bronchi, resulting in distal segmental collapse. Extrapulmonary findings are rare, but usually are in the form of calcified mediastinal adenopathy on CT-based imaging, which allows for differentiation from lung cancer. There is no reliable treatment though bronchodilators can achieve clinical benefit.
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PMID:Black lungs and big nodes: A case of airway anthracosis with bronchial anthracofibrosis. 2989 40