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Tongue swelling in the recovery room: a case report and discussion of postoperative angioedema
Journal of Clinical Anesthesia (2006) 18, 226 – 229
Case report
Tongue swelling in the recovery room: a case report and discussion of postoperative angioedema LoriJean K. Reed MD (Resident)*, Jin Meng MD, Girish P. Joshi MD (Professor) Department of Anesthesiology and Pain Management, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390-9068, USA Received 25 January 2005; accepted 22 August 2005
Keywords: Angioneurotic edema; Angiotensin-converting enzyme inhibitors; Postoperative care
Abstract We present a case of potentially life-threatening postoperative swelling of the tongue and oropharynx that developed in the postanesthesia care unit in a patient taking lisinopril. The principal treatment of angioedema is the discontinuation of the precipitating agent and airway management. Patients with swelling limited to the face and oral cavity may only require monitoring. However, those with swelling in the floor of the mouth, tongue, and supraglottic or glottic areas should have their airway secured by tracheal intubation immediately. Early intubation in patients displaying these characteristics may decrease the incidence of emergent surgical airways. Angioedema is self-limiting, and the swelling usually resolves spontaneously in two to 3 days. Proper identification of angiotensinconverting enzyme inhibitor–associated angioedema requiring a timely airway intervention may reduce mortality, and recognition of its self-limiting course can prevent unnecessary tracheostomy. D 2006 Elsevier Inc. All rights reserved.
1. Introduction Postoperative swelling of the tongue is a rare but potentially life-threatening situation. Cases of angioedema occurring in a patient on angiotensin-converting enzyme (ACE) inhibitor therapy after airway manipulation have been reported [1-5]. However, postoperative angioedema secondary to ACE inhibitor therapy has largely been overlooked by anesthesiologists. This may result in delayed recognition and unnecessary surgical airways [6]. We present a case of swelling in the tongue and oropharynx, which developed in the postanesthesia care unit (PACU). Differential diagnoses
* Corresponding author. Tel.: +1 214 590 7675; fax: +1 214 590 6945. E-mail address: [email protected] (L.J.K. Reed). 0952-8180/$ – see front matter D 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.jclinane.2005.08.019
of tongue and oropharynx swelling along with appropriate therapeutic interventions are discussed.
2. Case report A 51-year-old, 63-kg, 161-cm, African-American woman presented for an uvulopalatopharyngoplasty and bilateral tonsillectomy for obstructive sleep apnea. Her past medical history was significant for tobacco abuse, asthma, hypertension, diabetes mellitus, and gastroesophageal reflux disease. Her medications included inhaled albuterol, salmeterol, and fluticasone daily as well as lisinopril, metformin, esomeprazole, and estrogen. Her past surgical history included an uneventful hysterectomy and nasal septoplasty. She had no prior history of drug intolerance or allergic responses. Her vital signs, airway examination,
Tongue swelling in the recovery room
227 transferred to the intensive care unit. Her tongue continued to enlarge after her airway was secured (Fig. 1). Examination with the fiberoptic scope revealed edema in the supraglottic and glottic structures. In the intensive care unit, she remained intubated until her tongue size had significantly decreased. She also continued to receive dexamethasone, diphenhydramine, and ranitidine. Lisinopril was suspected to have precipitated the angioedema and was not restarted postoperatively. She was successfully extubated on postoperative day 2, and the swelling in her tongue completely resolved by the third day.
3. Discussion Fig. 1 View of patient’s enlarged tongue after her airway had been secured.
and the remainder of the physical examination were all unremarkable. Laboratory tests and electrocardiogram were also within normal limits. After application of routine monitoring devices and premedication with midazolam 2 mg intravenously (IV) and inhaled albuterol, anesthesia was induced with fentanyl and propofol IV. Tracheal intubation was facilitated using vecuronium and accomplished atraumatically on the first attempt. Anesthesia was maintained with sevoflurane and nitrous oxide in oxygen. Intraoperatively, she remained in a supine position, and fentanyl boluses were administered to maintain hemodynamic stability. She also received dexamethasone 8 mg. At the end of the surgical procedure, residual neuromuscular blockade was reversed with neostigmine and glycopyrrolate. The patient’s trachea was extubated in the operating room, and she was transferred to the PACU with supplemental oxygen in stable condition. The intraoperative course, lasting about an hour, was uneventful. Upon arrival in the PACU, she received fentanyl 50 lg IV for pain and ondansetron 4 mg IV for nausea. She also received clindamycin at the surgeon’s request. Approximately 1 1/2 hours after admission to the PACU, the nurse noticed some tongue swelling. The patient was awake and alert with stable vital signs. She received dexamethasone 8 mg, diphenhydramine 25 mg, and ranitidine 50 mg IV. In addition, the surgeon was asked to rule out any surgical causes for tongue swelling. Despite treatment, the patient’s tongue continued to enlarge in a symmetrical fashion. She was able to maintain a patent airway sitting in an upright position and was maintaining oxygen saturation above 95% on 100% humidified oxygen. At that time, epinephrine 0.5 mg IV was administered. Because her tongue continued to enlarge despite medical therapy, she was transferred to the operating room for an awake tracheal intubation. In the operating room, surgical and nursing personnel were prepared for a surgical airway. The patient’s trachea was intubated nasally without difficulty, and her care was
The differential diagnosis of postoperative tongue swelling includes angioedema, allergic reaction and anaphylaxis, hematoma formation, and tongue congestion secondary to traumatic or prolonged compression during surgery. Our patient’s presentation was devoid of systemic symptoms, hypotension, or dermatologic manifestations seen during an allergic or anaphylactic reaction. A discrete, hard, discolored mass was not present to indicate a hematoma had formed. Tissue congestion caused by the surgical instruments or procedure was discounted because the patient demonstrated swelling around her eyes, and examination with the fiberoptic scope revealed edema in the supraglottic and glottic structures. The surgical instruments did not directly disturb these areas. Our patient did demonstrate a symmetric, soft, nonpitting edema, that is characteristic of angioedema. She also had 3 predisposing conditions that make angioedema a reasonable diagnosis. The patient was taking an ACE inhibitor, a class of antihypertensive medications well known to cause angioedema [7-9]. Moreover, airway manipulation has been reported to precipitate ACE inhibitor angioedema [1-5]. Furthermore, people of the African-American race are also at a higher risk of developing ACE inhibitor–induced angioedema [10-12]. She also had a history of sleep apnea, which placed her at a greater risk for upper airway obstruction secondary to ACE inhibitor–induced angioedema [13]. Extravasation of plasma secondary to an increase in vascular permeability and vasodilatation is believed to cause angioedema. This may result from the activation of the kallikrein-kinin system and classic complement pathway leading to release of bradykinin, kallidin, and anaphylatoxins. This manifests clinically as a nonpitting edema of the mucosa of the airway and gastrointestinal tract and/or the deeper layers of the skin most commonly on the face [7,8]. The inciting event of the inflammatory cascade leading to angioedema is sometimes idiopathic [14]. However, angioedema has been associated with certain medications, allergens, physical trauma, and hereditary or acquired autoimmune abnormalities in the complement system. Medications that have been implicated include antibiotics, opioids, nonsteroidal anti-inflammatory drugs, ACE inhibitors, and angiotensin
228
L.J.K. Reed et al.
Table 1 Classification of angioedema as described by Chiu et al [12] Pattern
Clinical description
Management
Type 1
Swelling is limited to face and oral cavity and excludes the floor of the mouth Swelling extends to the floor of the mouth, tongue, soft palate, and/or uvula
May be observed on the ward
Type 2
Type 3
Swelling extends to supraglottic and glottic structures
Close observation in the intensive care unit. If severe, proceed to fiberoptic intubation. Close observation in the intensive care unit. If severe, proceed to fiberoptic intubation.
II receptor antagonists. Accounting for 38% to 68% of all cases, ACE inhibitor–associated angioedema is the most common cause of angioedema [12,15]. The incidence of ACE inhibitor-associated angioedema is one to two in 1000 [9,15]. The development of angioedema in a patient taking ACE inhibitors can occur early (weeks) or late (years) in the course of therapy [7-9]. Associated mortality is currently high at 11% [15]. The mechanism of angioedema in patients taking ACE inhibitors is not fully understood. It is thought to be secondary to an increase in kinins. Supporting this theory is the observation that patients taking ACE inhibitors with a genetic deficiency in aminopeptidase P, an enzyme involved in kinin degradation, are predisposed to this complication [16]. Confusing the picture is that angiotensin II receptor antagonists have been associated with angioedema, but antagonizing the angiotensin II receptor does not raise kinin levels [17]. Hereditary and acquired forms of C1 esterase inhibitor deficiency/dysfunction exist, and these patients are susceptible to developing acute swelling after dental or surgical manipulation [7,8]. Our patient’s complement system was determined to be normal by measurements of C4, C1q, and a quantitative and functional assay of C1 esterase inhibitor. The principal treatment of angioedema is the discontinuation of the precipitating agent and airway management [12]. Angioedema is self-limiting, and the swelling usually resolves spontaneously for two to 3 days [7,8,12]. Proper identification of angioedema requiring airway intervention could reduce mortality, and recognition of its self-limiting course can prevent unnecessary surgical airways. Chiu et al [12] presented an algorithm for airway management based on classifying the symptoms of angioedema into 3 types. It has been recommended that a patient with severe type 2 or type 3 angioedema should have their airway secured by tracheal intubation (Table 1). In the series of Chiu et al, 21% of type 2 and 33% of type 3 angioedema patients required intubation. Our patient had characteristics of type 3
angioedema (tongue, floor of the mouth, and glottic and supraglottic swelling) so that securing her airway with tracheal intubation was indicated. In treating angioedema of all etiologies, steroids, antihistamines, epinephrine, and humidified oxygen are widely used. However, they have not been shown convincingly to provide any benefit [7,8]. In cases of hereditary or acquired autoimmune angioedema, androgens that increase the serum concentration of C1 esterase inhibitor such as danazol and stanozolol may be of benefit [8]. Administration of C1 esterase inhibitor concentrate (not available in the United States) is successful in cases of hereditary, but not acquired angioedema [8]. Fresh frozen plasma is not recommended. Although it contains C1 esterase inhibitor, it also contains C4, which could lead to the continuing activation of the complement system [8]. In summary, there should be a high index of suspicion for angioedema in a patient with tongue swelling in the immediate postoperative period. It is important to recognize patterns of swelling and to be familiar with the differential diagnosis of tongue edema to care for patients with this serious complication. Expedient assessment of the airway and appropriate intervention may prevent mortality and morbidity associated with late recognition of airway compromise.
References [1] Aziz SR, Tin P. Spontaneous angioedema of oral cavity after dental impressions. N Y State Dent J 2002;69:42 - 5. [2] Kharasch ED. Angiotensin-converting enzyme inhibitor–induced angioedema associated with endotracheal intubation. Anesth Analg 1992;74:602 - 4. [3] Ogbureke KU, Cruz C, Johnson JV, Helfrick JF. Perioperative angioedema in a patient on long-term angiotensin-converting enzyme inhibitor therapy. J Oral Maxillofac Surg 1996;54:917 - 20. [4] Peacock ME, Brennan WA, Strong SL, et al. Angioedema as a complication in periodontal surgery: report of a case. J Periodontol 1991;62:643 - 5. [5] Sadeghi N, Panje WR. Life-threatening perioperative angioedema related to angiotensin-converting enzyme inhibitor therapy. J Otolaryngol 1999;28:354 - 6. [6] Rai MR, Amen F, Idrees F. Angiotensin-converting enzyme inhibitor related angioedema and the anaesthetist. Anaesthesia 2004;59:283 - 9. [7] Frank MM. Urticaria and angioedema. In: Goldman L, Bennett JC, editors. Cecil Textbook of Medicine, 21st ed. Philadelphia7 W.B. Saunders; 2000. p. 1440 - 5. [8] Frigas E, Nzeako UC. Angioedema pathogenesis, differential diagnosis and treatment. Clin Rev Allergy Immunol 2002;23:217 - 31. [9] Inman WH, Rawson NS, Wilton LV, et al. Postmarketing surveillance of enalapril. BMJ 1988;297:826 - 9. [10] Brown NJ, Ray WA, Snowden M, Griffin MR. Black Americans have an increased rate of angiotensin converting enzyme inhibitor– associated angioedema. Clin Pharmacol Ther 1996;60:8 - 13. [11] Gainer JV, Nadeau JH, Ryder D, et al. Increased sensitivity to bradykinin among African Americans. J Allergy Clin Immunol 1996; 98:283 - 7. [12] Chiu AG, Newkirk KA, Davidson BJ, et al. Angiotensin-converting enzyme inhibitor–induced angioedema: a multi-center review and an algorithm for airway management. Ann Otol Rhinol Laryngol 2001; 110:834 - 40.
Tongue swelling in the recovery room [13] Jain M, Armstrong L, Hall J. Predisposition to and late onset of upper airway obstruction following angiotensin-converting enzyme inhibitor therapy. Chest 1992;102:871 - 4. [14] Krnacik MJ, Heggeness MH. Severe angioedema causing airway obstruction after anterior cervical surgery. Spine 1997;22:2188 - 90. [15] Agah R, Bandi V, Guntupalli KK. Angioedema: the role of ACE inhibitors and factors associated with poor clinical outcome. Intensive Care Med 1997;23:793 - 6.
229 [16] Adam A, Cugno M, Molinaro G, et al. Aminopeptidase P in individuals with a history of angioedema on ACE inhibitors. Lancet 2002;359:2088 - 9. [17] Chiu AG, Krowiak EJ, Deeb ZE. Angioedema associated with angiotensin II receptor antagonists: challenging our knowledge of angioedema and its etiology. Laryngoscope 2001;111:1729 - 31.
Case report
Tongue swelling in the recovery room: a case report and discussion of postoperative angioedema LoriJean K. Reed MD (Resident)*, Jin Meng MD, Girish P. Joshi MD (Professor) Department of Anesthesiology and Pain Management, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390-9068, USA Received 25 January 2005; accepted 22 August 2005
Keywords: Angioneurotic edema; Angiotensin-converting enzyme inhibitors; Postoperative care
Abstract We present a case of potentially life-threatening postoperative swelling of the tongue and oropharynx that developed in the postanesthesia care unit in a patient taking lisinopril. The principal treatment of angioedema is the discontinuation of the precipitating agent and airway management. Patients with swelling limited to the face and oral cavity may only require monitoring. However, those with swelling in the floor of the mouth, tongue, and supraglottic or glottic areas should have their airway secured by tracheal intubation immediately. Early intubation in patients displaying these characteristics may decrease the incidence of emergent surgical airways. Angioedema is self-limiting, and the swelling usually resolves spontaneously in two to 3 days. Proper identification of angiotensinconverting enzyme inhibitor–associated angioedema requiring a timely airway intervention may reduce mortality, and recognition of its self-limiting course can prevent unnecessary tracheostomy. D 2006 Elsevier Inc. All rights reserved.
1. Introduction Postoperative swelling of the tongue is a rare but potentially life-threatening situation. Cases of angioedema occurring in a patient on angiotensin-converting enzyme (ACE) inhibitor therapy after airway manipulation have been reported [1-5]. However, postoperative angioedema secondary to ACE inhibitor therapy has largely been overlooked by anesthesiologists. This may result in delayed recognition and unnecessary surgical airways [6]. We present a case of swelling in the tongue and oropharynx, which developed in the postanesthesia care unit (PACU). Differential diagnoses
* Corresponding author. Tel.: +1 214 590 7675; fax: +1 214 590 6945. E-mail address: [email protected] (L.J.K. Reed). 0952-8180/$ – see front matter D 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.jclinane.2005.08.019
of tongue and oropharynx swelling along with appropriate therapeutic interventions are discussed.
2. Case report A 51-year-old, 63-kg, 161-cm, African-American woman presented for an uvulopalatopharyngoplasty and bilateral tonsillectomy for obstructive sleep apnea. Her past medical history was significant for tobacco abuse, asthma, hypertension, diabetes mellitus, and gastroesophageal reflux disease. Her medications included inhaled albuterol, salmeterol, and fluticasone daily as well as lisinopril, metformin, esomeprazole, and estrogen. Her past surgical history included an uneventful hysterectomy and nasal septoplasty. She had no prior history of drug intolerance or allergic responses. Her vital signs, airway examination,
Tongue swelling in the recovery room
227 transferred to the intensive care unit. Her tongue continued to enlarge after her airway was secured (Fig. 1). Examination with the fiberoptic scope revealed edema in the supraglottic and glottic structures. In the intensive care unit, she remained intubated until her tongue size had significantly decreased. She also continued to receive dexamethasone, diphenhydramine, and ranitidine. Lisinopril was suspected to have precipitated the angioedema and was not restarted postoperatively. She was successfully extubated on postoperative day 2, and the swelling in her tongue completely resolved by the third day.
3. Discussion Fig. 1 View of patient’s enlarged tongue after her airway had been secured.
and the remainder of the physical examination were all unremarkable. Laboratory tests and electrocardiogram were also within normal limits. After application of routine monitoring devices and premedication with midazolam 2 mg intravenously (IV) and inhaled albuterol, anesthesia was induced with fentanyl and propofol IV. Tracheal intubation was facilitated using vecuronium and accomplished atraumatically on the first attempt. Anesthesia was maintained with sevoflurane and nitrous oxide in oxygen. Intraoperatively, she remained in a supine position, and fentanyl boluses were administered to maintain hemodynamic stability. She also received dexamethasone 8 mg. At the end of the surgical procedure, residual neuromuscular blockade was reversed with neostigmine and glycopyrrolate. The patient’s trachea was extubated in the operating room, and she was transferred to the PACU with supplemental oxygen in stable condition. The intraoperative course, lasting about an hour, was uneventful. Upon arrival in the PACU, she received fentanyl 50 lg IV for pain and ondansetron 4 mg IV for nausea. She also received clindamycin at the surgeon’s request. Approximately 1 1/2 hours after admission to the PACU, the nurse noticed some tongue swelling. The patient was awake and alert with stable vital signs. She received dexamethasone 8 mg, diphenhydramine 25 mg, and ranitidine 50 mg IV. In addition, the surgeon was asked to rule out any surgical causes for tongue swelling. Despite treatment, the patient’s tongue continued to enlarge in a symmetrical fashion. She was able to maintain a patent airway sitting in an upright position and was maintaining oxygen saturation above 95% on 100% humidified oxygen. At that time, epinephrine 0.5 mg IV was administered. Because her tongue continued to enlarge despite medical therapy, she was transferred to the operating room for an awake tracheal intubation. In the operating room, surgical and nursing personnel were prepared for a surgical airway. The patient’s trachea was intubated nasally without difficulty, and her care was
The differential diagnosis of postoperative tongue swelling includes angioedema, allergic reaction and anaphylaxis, hematoma formation, and tongue congestion secondary to traumatic or prolonged compression during surgery. Our patient’s presentation was devoid of systemic symptoms, hypotension, or dermatologic manifestations seen during an allergic or anaphylactic reaction. A discrete, hard, discolored mass was not present to indicate a hematoma had formed. Tissue congestion caused by the surgical instruments or procedure was discounted because the patient demonstrated swelling around her eyes, and examination with the fiberoptic scope revealed edema in the supraglottic and glottic structures. The surgical instruments did not directly disturb these areas. Our patient did demonstrate a symmetric, soft, nonpitting edema, that is characteristic of angioedema. She also had 3 predisposing conditions that make angioedema a reasonable diagnosis. The patient was taking an ACE inhibitor, a class of antihypertensive medications well known to cause angioedema [7-9]. Moreover, airway manipulation has been reported to precipitate ACE inhibitor angioedema [1-5]. Furthermore, people of the African-American race are also at a higher risk of developing ACE inhibitor–induced angioedema [10-12]. She also had a history of sleep apnea, which placed her at a greater risk for upper airway obstruction secondary to ACE inhibitor–induced angioedema [13]. Extravasation of plasma secondary to an increase in vascular permeability and vasodilatation is believed to cause angioedema. This may result from the activation of the kallikrein-kinin system and classic complement pathway leading to release of bradykinin, kallidin, and anaphylatoxins. This manifests clinically as a nonpitting edema of the mucosa of the airway and gastrointestinal tract and/or the deeper layers of the skin most commonly on the face [7,8]. The inciting event of the inflammatory cascade leading to angioedema is sometimes idiopathic [14]. However, angioedema has been associated with certain medications, allergens, physical trauma, and hereditary or acquired autoimmune abnormalities in the complement system. Medications that have been implicated include antibiotics, opioids, nonsteroidal anti-inflammatory drugs, ACE inhibitors, and angiotensin
228
L.J.K. Reed et al.
Table 1 Classification of angioedema as described by Chiu et al [12] Pattern
Clinical description
Management
Type 1
Swelling is limited to face and oral cavity and excludes the floor of the mouth Swelling extends to the floor of the mouth, tongue, soft palate, and/or uvula
May be observed on the ward
Type 2
Type 3
Swelling extends to supraglottic and glottic structures
Close observation in the intensive care unit. If severe, proceed to fiberoptic intubation. Close observation in the intensive care unit. If severe, proceed to fiberoptic intubation.
II receptor antagonists. Accounting for 38% to 68% of all cases, ACE inhibitor–associated angioedema is the most common cause of angioedema [12,15]. The incidence of ACE inhibitor-associated angioedema is one to two in 1000 [9,15]. The development of angioedema in a patient taking ACE inhibitors can occur early (weeks) or late (years) in the course of therapy [7-9]. Associated mortality is currently high at 11% [15]. The mechanism of angioedema in patients taking ACE inhibitors is not fully understood. It is thought to be secondary to an increase in kinins. Supporting this theory is the observation that patients taking ACE inhibitors with a genetic deficiency in aminopeptidase P, an enzyme involved in kinin degradation, are predisposed to this complication [16]. Confusing the picture is that angiotensin II receptor antagonists have been associated with angioedema, but antagonizing the angiotensin II receptor does not raise kinin levels [17]. Hereditary and acquired forms of C1 esterase inhibitor deficiency/dysfunction exist, and these patients are susceptible to developing acute swelling after dental or surgical manipulation [7,8]. Our patient’s complement system was determined to be normal by measurements of C4, C1q, and a quantitative and functional assay of C1 esterase inhibitor. The principal treatment of angioedema is the discontinuation of the precipitating agent and airway management [12]. Angioedema is self-limiting, and the swelling usually resolves spontaneously for two to 3 days [7,8,12]. Proper identification of angioedema requiring airway intervention could reduce mortality, and recognition of its self-limiting course can prevent unnecessary surgical airways. Chiu et al [12] presented an algorithm for airway management based on classifying the symptoms of angioedema into 3 types. It has been recommended that a patient with severe type 2 or type 3 angioedema should have their airway secured by tracheal intubation (Table 1). In the series of Chiu et al, 21% of type 2 and 33% of type 3 angioedema patients required intubation. Our patient had characteristics of type 3
angioedema (tongue, floor of the mouth, and glottic and supraglottic swelling) so that securing her airway with tracheal intubation was indicated. In treating angioedema of all etiologies, steroids, antihistamines, epinephrine, and humidified oxygen are widely used. However, they have not been shown convincingly to provide any benefit [7,8]. In cases of hereditary or acquired autoimmune angioedema, androgens that increase the serum concentration of C1 esterase inhibitor such as danazol and stanozolol may be of benefit [8]. Administration of C1 esterase inhibitor concentrate (not available in the United States) is successful in cases of hereditary, but not acquired angioedema [8]. Fresh frozen plasma is not recommended. Although it contains C1 esterase inhibitor, it also contains C4, which could lead to the continuing activation of the complement system [8]. In summary, there should be a high index of suspicion for angioedema in a patient with tongue swelling in the immediate postoperative period. It is important to recognize patterns of swelling and to be familiar with the differential diagnosis of tongue edema to care for patients with this serious complication. Expedient assessment of the airway and appropriate intervention may prevent mortality and morbidity associated with late recognition of airway compromise.
References [1] Aziz SR, Tin P. Spontaneous angioedema of oral cavity after dental impressions. N Y State Dent J 2002;69:42 - 5. [2] Kharasch ED. Angiotensin-converting enzyme inhibitor–induced angioedema associated with endotracheal intubation. Anesth Analg 1992;74:602 - 4. [3] Ogbureke KU, Cruz C, Johnson JV, Helfrick JF. Perioperative angioedema in a patient on long-term angiotensin-converting enzyme inhibitor therapy. J Oral Maxillofac Surg 1996;54:917 - 20. [4] Peacock ME, Brennan WA, Strong SL, et al. Angioedema as a complication in periodontal surgery: report of a case. J Periodontol 1991;62:643 - 5. [5] Sadeghi N, Panje WR. Life-threatening perioperative angioedema related to angiotensin-converting enzyme inhibitor therapy. J Otolaryngol 1999;28:354 - 6. [6] Rai MR, Amen F, Idrees F. Angiotensin-converting enzyme inhibitor related angioedema and the anaesthetist. Anaesthesia 2004;59:283 - 9. [7] Frank MM. Urticaria and angioedema. In: Goldman L, Bennett JC, editors. Cecil Textbook of Medicine, 21st ed. Philadelphia7 W.B. Saunders; 2000. p. 1440 - 5. [8] Frigas E, Nzeako UC. Angioedema pathogenesis, differential diagnosis and treatment. Clin Rev Allergy Immunol 2002;23:217 - 31. [9] Inman WH, Rawson NS, Wilton LV, et al. Postmarketing surveillance of enalapril. BMJ 1988;297:826 - 9. [10] Brown NJ, Ray WA, Snowden M, Griffin MR. Black Americans have an increased rate of angiotensin converting enzyme inhibitor– associated angioedema. Clin Pharmacol Ther 1996;60:8 - 13. [11] Gainer JV, Nadeau JH, Ryder D, et al. Increased sensitivity to bradykinin among African Americans. J Allergy Clin Immunol 1996; 98:283 - 7. [12] Chiu AG, Newkirk KA, Davidson BJ, et al. Angiotensin-converting enzyme inhibitor–induced angioedema: a multi-center review and an algorithm for airway management. Ann Otol Rhinol Laryngol 2001; 110:834 - 40.
Tongue swelling in the recovery room [13] Jain M, Armstrong L, Hall J. Predisposition to and late onset of upper airway obstruction following angiotensin-converting enzyme inhibitor therapy. Chest 1992;102:871 - 4. [14] Krnacik MJ, Heggeness MH. Severe angioedema causing airway obstruction after anterior cervical surgery. Spine 1997;22:2188 - 90. [15] Agah R, Bandi V, Guntupalli KK. Angioedema: the role of ACE inhibitors and factors associated with poor clinical outcome. Intensive Care Med 1997;23:793 - 6.
229 [16] Adam A, Cugno M, Molinaro G, et al. Aminopeptidase P in individuals with a history of angioedema on ACE inhibitors. Lancet 2002;359:2088 - 9. [17] Chiu AG, Krowiak EJ, Deeb ZE. Angioedema associated with angiotensin II receptor antagonists: challenging our knowledge of angioedema and its etiology. Laryngoscope 2001;111:1729 - 31.