두경부 혈관부종에 대한 임상적 고찰 = Clinical Analysis of Angioedema of the Head and Neck

다국어 초록 (Multilingual Abstract)

Angioedema is a localized, nonpitting edema resulting from extravasation of fluid into the
interstitial space. It usually develops suddenly and fades during the course of 24 to 48 hours. However, angioedema of the upper
respiratory tract can result in serious acute respiratory distress, airway obstruction, and death. The purpose of this study was to
analyze clinical characteristics of angioedema in the head and neck. Subjects and Method：A review of 144 patients with angioedema
of the head and neck over 3-year period was conducted. Results：The presumptive causes were 115 allergic reactions
to food, drug, or environmental exposure, 3 losses of C1 esterase inhibitor, 1 angiotensin-converting enzyme inhibitor use, and 25
idiopathic conditions. The main locations of the edema were 100 face/lips, 4 oral cavity/oropharynx, 5 larynx/hypopharynx, and
35 multiple sites of the head and neck. Most of patients were treated with steroids and H1 and H2 blockers. All of 7 patients with
low oxygen saturation and 14 out of 18 patients with hypotension on arrival were improved within 24 hours. There were 4 patients
with airway distress treated with urgent airway intervention, three of them were completely recovered within 110-240
hours but one of them died of the disease. Patients with the cause of idiopathic and loss of C1 esterase inhibitor were found to
stay longer in the hospital over 48 hours (p<0.05). Conclusion：Angioedema of the head and neck usually responds well to the
treatment. However, there might be cases with life-threatening airway obstruction. (Korean J Otorhinolaryngol-Head Neck
Surg 2008;51:726-30)

참고문헌 (Reference)

1 Kyrmizakis DE, "Skoulas JG. Tongue angioedema after long-term use of ACE inhibitors" 19 (19): 394-396, 1998

2 Zirkle M, "Predictors of airway intervention in angioedema of the head and neck" 123 (123): 240-245, 2000

3 Ishoo E, "Predicting airway risk in angioedema: Staging system based on presentation" 121 (121): 263-268, 1999

4 Shah UK, "Pediatric angioedema: Ten years’ experience" 125 (125): 791-795, 1999

5 Pruet CW, "Management of the airway in patients with angioedema" 93 (93): 749-755, 1983

6 Barna JS, "Life-threatening angioedema" 103 (103): 795-798, 1990

7 Goldberg R, "Evaluation and management of acute uvular edema" 22 (22): 251-255, 1993

8 Thompson T, "Drug-induced, life-threatening angioedema revisited" 103 (103): 10-12, 1993

9 Israili ZH, "Cough and angioneurotic edema associated with angiotensin-converting enzyme inhibitor therapy" 117 (117): 234-242, 1992

10 Slater EE, "Clinical profile of angioedema associated with angiotensin converting-enzyme inhibition" 260 (260): 967-970, 1988

11 김위황, "C1 Inhibitor 결핍 증후군 1예" 대한이비인후과학회 45 (45): 191-194, 2002

12 Sabore RA, "Angiotensin-converting enzyme (ACE) inhibitors and angio-oedema" 136 (136): 153-158, 1997

13 Gunkel AR, "Angioneurotic edema as a reaction to angiotensin-converting enzyme inhibitors" 17 (17): 87-91, 1996

14 Agah R, "Angioedema: The role of ACE inhibitors and factors associated with poor clinical outcome" 23 (23): 793-796, 1997

15 Megerian CA, "Angioedema: 5 years’ expe Korean J Otorhinolaryngol-Head 730 Neck Surg 2008;51:726-30 rience, with a review of the disorder’s presentation and treatment" 102 (102): 256-260, 1992

16 Seidman MD, "Angioedema related to angiotensin-converting enzyme inhibitors" 102 (102): 727-731, 1990