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代谢性酸中毒作为重度急性哮喘患儿呼吸窘迫的潜在机制。

Metabolic acidosis as an underlying mechanism of respiratory distress in children with severe acute asthma.

作者信息

Meert Kathleen L, Clark Jeff, Sarnaik Ashok P

机构信息

Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, MI, USA.

出版信息

Pediatr Crit Care Med. 2007 Nov;8(6):519-23. doi: 10.1097/01.PCC.0000288673.82916.9D.

Abstract

OBJECTIVE

  1. To alert the clinician that increasing rate and depth of breathing during treatment of acute asthma may be a manifestation of metabolic acidosis with hyperventilation rather than worsening airway obstruction; and 2) to describe the frequency of metabolic acidosis with hyperventilation in children with severe acute asthma admitted to our pediatric intensive care unit.

DESIGN

Retrospective medical record review.

SETTING

University-affiliated children's hospital.

PATIENTS

All patients admitted to the pediatric intensive care unit with a diagnosis of asthma between January 1, 2005, and December 31, 2005.

INTERVENTIONS

None.

MEASUREMENTS AND MAIN RESULTS

Fifty-three patients with asthma (median age 7.8 yrs, range 0.7-17.9 yrs; 35 [66%] male; 46 [87%] black and 7 [13%] white) were admitted to the pediatric intensive care unit during the study period. Fifteen (28%) patients developed metabolic acidosis with hyperventilation (pH <7.35, Pco2 <35 torr [4.6 kPa], and base excess < or = -7 mmol/L) during their hospital course. Of these, lactic acid was assessed in four patients and was elevated in each; all had hyperglycemia (blood glucose >120 mg/dL [6.7 mmol/L]). Patients who developed metabolic acidosis with hyperventilation received asthma therapy similar to that received by patients who did not develop the disorder. Metabolic acidosis resolved contemporaneously with tapering of beta2-adrenergic agonists and administration of supportive care. All patients survived.

CONCLUSIONS

Metabolic acidosis with hyperventilation manifesting as respiratory distress can occur in children with severe acute asthma. A pathophysiologic rationale exists for the contribution of beta2-adrenergic agents to the development of this acid-base disorder. Failure to recognize metabolic acidosis as the underlying mechanism of respiratory distress may lead to inappropriate intensification of bronchodilator therapy. Supportive care and tapering of beta2-adrenergic agents are recommended to resolve this condition.

摘要

目的

1)提醒临床医生,急性哮喘治疗期间呼吸频率和深度增加可能是代谢性酸中毒伴过度通气的表现,而非气道阻塞加重;2)描述入住我院儿科重症监护病房的重症急性哮喘患儿中代谢性酸中毒伴过度通气的发生率。

设计

回顾性病历审查。

地点

大学附属医院儿童医院。

患者

2005年1月1日至2005年12月31日期间入住儿科重症监护病房且诊断为哮喘的所有患者。

干预措施

无。

测量指标及主要结果

研究期间,53例哮喘患者(中位年龄7.8岁,范围0.7 - 17.9岁;35例[66%]为男性;46例[87%]为黑人,7例[13%]为白人)入住儿科重症监护病房。15例(28%)患者在住院期间出现代谢性酸中毒伴过度通气(pH <7.35,二氧化碳分压<35托[4.6千帕],碱剩余≤ -7毫摩尔/升)。其中,4例患者检测了乳酸,均升高;所有患者均有高血糖(血糖>120毫克/分升[6.7毫摩尔/升])。发生代谢性酸中毒伴过度通气的患者接受的哮喘治疗与未发生该病症的患者相似。代谢性酸中毒在β2肾上腺素能激动剂逐渐减量并给予支持治疗的同时得到缓解。所有患者均存活。

结论

重症急性哮喘患儿可出现表现为呼吸窘迫的代谢性酸中毒伴过度通气。β2肾上腺素能药物导致这种酸碱紊乱的发生存在病理生理学依据。未能认识到代谢性酸中毒是呼吸窘迫的潜在机制可能导致支气管扩张剂治疗不适当的强化。建议采取支持治疗并逐渐减少β2肾上腺素能药物的用量以缓解这种情况。

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