Blum Richard H, McGowan Francis X
Department of Anesthesia, Perioperative and Pain Medicine, Children's Hospital, Boston and Harvard Medical School, Boston, MA 02115, USA.
Paediatr Anaesth. 2004 Jan;14(1):75-83. doi: 10.1046/j.1460-9592.2003.01193.x.
The causes of obstruction to airflow in the pediatric upper airway include craniofacial disorders, subglottic stenosis, choanal atresia, syndromes associated with neuromuscular weakness, and the most common, hypertrophy of the tonsils and adenoids. Abnormal breathing can adversely affect craniofacial growth, and abnormal craniofacial development can promote upper airway obstruction. Chronic upper airway obstruction often presents with evidence of obstructive sleep apnea syndrome; in severe cases these children also present with pulmonary hypertension and cor pulmonale. The development of pulmonary hypertension and right heart dysfunction from chronic upper airway obstruction is complex. Hypoxemia and hypercarbia-induced respiratory acidosis are potent mediators of pulmonary vasoconstriction that can lead to reversible and irreversible chronic changes in the pulmonary vasculature. It is likely that production of various neurohumoral factors in response to hypoxemia and respiratory distress may further promote pulmonary hypertension, right ventricular dysfunction, and consequent impairment of systemic cardiac output. The anesthetic considerations for children undergoing adenotonsillectomy for chronic airway obstruction are significant. These children are at high risk for complications such as laryngospasm, desaturation, stimulation of pulmonary hypertension and cardiac dysfunction, pulmonary edema, postoperative upper airway obstruction, and respiratory arrest. Because of underlying condition(s) (facial abnormalities, neuromuscular disease, etc.), successful adenotonsillar surgery may not improve upper airway obstruction significantly, especially in the immediate postoperative period when edema, bleeding and the effects of anesthetics and analgesics are present.
小儿上气道气流阻塞的原因包括颅面疾病、声门下狭窄、后鼻孔闭锁、与神经肌肉无力相关的综合征，以及最常见的扁桃体和腺样体肥大。异常呼吸会对颅面生长产生不利影响，而异常的颅面发育会加重上气道阻塞。慢性上气道阻塞常表现为阻塞性睡眠呼吸暂停综合征；严重时，这些患儿还会出现肺动脉高压和肺心病。慢性上气道阻塞导致肺动脉高压和右心功能障碍的机制较为复杂。低氧血症和高碳酸血症引起的呼吸性酸中毒是肺血管收缩的重要介质，可导致肺血管系统发生可逆和不可逆的慢性改变。低氧血症和呼吸窘迫引发的各种神经体液因子的产生，可能会进一步加重肺动脉高压、右心室功能障碍，进而损害全身心输出量。对于因慢性气道阻塞接受腺样体扁桃体切除术的患儿，麻醉方面的考虑至关重要。这些患儿发生喉痉挛、低氧血症、肺动脉高压和心功能障碍、肺水肿、术后上气道阻塞及呼吸骤停等并发症的风险较高。由于存在潜在疾病（面部畸形、神经肌肉疾病等），成功的腺样体扁桃体手术可能无法显著改善上气道阻塞，尤其是在术后早期，此时存在水肿、出血以及麻醉药和镇痛药的影响。
