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  • Appropriate management of TLS includes risk assessment

    2018-11-02

    Appropriate management of TLS includes risk assessment, fluid management for TLS prophylaxis, and drug therapy. Fluid management is the key to TLS prevention. Aggressive hydration and maintenance of normal urine output are important in decreasing uric Stem Cell Compound Library deposition in the renal tubules to prevent acute urate nephropathy. Diuretics can be administered when urine output maintenance is required. Allopurinol is used to prevent the formation of uric acid by inhibition of xanthine oxidase, which converts xanthine into hypoxanthine and then into uric acid. However, allopurinol is ineffective in reducing uric acid levels and increasing the xanthine and hypoxanthine levels; it can also promote obstructive uropathy. Rasburicase reduces serum uric acid levels more rapidly than allopurinol via enzymatic degradation of uric acid to allantoin, which is highly soluble. Rasburicase is an FDA-approved drug for the management of patients with malignancies who are receiving anticancer therapy that could result in TLS. Urine alkalinization (maintaining urine pH > 7) is used to increase the solubility of uric acid in urine to decrease potential deposition of urate crystals. One disadvantage of urine alkalinization is that it increases the risk of calcium phosphate deposition in the kidney. Therefore, urine alkalinization is suggested only for patients with metabolic acidosis. Electrolyte monitoring in patients undergoing cytotoxic therapy and rapid appropriate therapeutic intervention are important. Ultimately, dialysis may be needed if severe renal failure, electrolyte imbalance, and metabolic derangement occur.
    Introduction Bronchogenic cysts are congenital anomalies believed, from an embryological aspect, to originate from abnormal budding of the tracheobronchial component during foregut development. The final location is related to the timing of budding, and most bronchogenic cysts are located in the mediastinum and remain asymptomatic. Neck bronchogenic cysts are rare and are generally detected in childhood. They are often found incidentally at an early age, but may have symptoms including stridor in neonates, dyspnea on exertion, dysphagia, and recurrent infection. Only two cases of neck abscess complicating neck bronchogenic cyst have been reported previously. Here, we report a case of a large neck abscess arising from a bronchogenic cyst in an adult. The patient underwent surgical excision, and no recurrence was noted during a 12-month follow-up period.
    Case report A 67-year-old woman was referred to our hospital for evaluation of neck pain with dysphagia. She had suffered from progressive dysphagia and sore throat for 5 days before admission. There was no history of any systemic disease. On examination, the body temperature was 37.3°C, the systolic and diastolic blood pressures were 124 and 82 mmHg, respectively, the pulse was 106 beats/minute, and the respiratory rate was normal. A protruding soft mass without obvious local heat measuring approximately 3 cm in diameter was located in the suprasternal area. The patient reported mild pain during palpation. There were no palpable neck lymph nodes or other oropharyngeal lesions. Leukocytosis (white blood cells: 17.76 103/μL; segmented: 86.6%) was noted, but the remainder of the complete blood count, urinalysis, and serum levels of electrolytes were within normal limits. Plain radiographs of the chest showed a localized air–fluid interface in the upper mediastinum (Fig. 1), and a computed tomography (CT) scan revealed a 5-cm cystic lesion containing an air–fluid level located near the trachea and esophagus (Fig. 2A), extending from the neck to the thoracic inlet (Fig. 2B). The trachea and esophagus were displaced to the left side (Fig. 2C). Cervical abscess of unknown origin was suspected, and possible causes were esophageal leakage and infection of a diverticulum; however, a subsequent esophagography revealed no visible fistula or diverticulum formation (Fig. 2D). Echo-guided needle aspiration was performed, and pus-like fluid was aspirated for cytology and culture examinations. A cytological examination yielded numerous polymorphonuclear leukocytes and scant histiocytes and ciliated columnar cells; Gram staining revealed only pus cell without any visible bacteria (Fig. 3A). The cyst was surgically removed through a paramidline incision with blunt dissection from the surrounding anatomical structures including the sternocleidomastoid muscle, common carotid artery, external jugular vein, and vagus and recurrent laryngeal nerves. A histopathological examination was performed, which revealed a bronchogenic cyst composed of fibrotic stroma lined by ciliated respiratory epithelium with a fibrinopurulent exudative coating (Fig. 3B). Acute and chronic inflammation, lymphoid follicles, hemorrhage, necrosis, and granulation tissue formation were also seen. Postoperatively, the patient suffered unilateral vocal cord palsy with voice change, but no swallowing disorder was noted on postoperative esophagography. The hoarseness resolved without treatment 10 months later.