Pulmonary Edema due to Upper Airway Obstruction in Adults
1988; Elsevier BV; Volume: 94; Issue: 5 Linguagem: Inglês
10.1378/chest.94.5.1090
ISSN1931-3543
Autores Tópico(s)Healthcare Decision-Making and Restraints
ResumoA report of pulmonary edema following acute upper airway obstruction in an adult is presented, and the literature involving 25 additional cases is reviewed. This form of pulmonary edema appears to be related to markedly negative intrathoracic pressure due to forced inspiration against a closed upper airway resulting in transudation of fluid from pulmonary capillaries to the interstitium. Postanesthetic laryngospasm is the most common cause of pulmonary edema in adults (11/26 cases). The edema usually clears rapidly with supportive care. Aggressive diagnostic and therapeutic interventions may be avoided if the syndrome is recognized. Maintenance of oxygenation and a patent airway are the mainstays of treatment. A report of pulmonary edema following acute upper airway obstruction in an adult is presented, and the literature involving 25 additional cases is reviewed. This form of pulmonary edema appears to be related to markedly negative intrathoracic pressure due to forced inspiration against a closed upper airway resulting in transudation of fluid from pulmonary capillaries to the interstitium. Postanesthetic laryngospasm is the most common cause of pulmonary edema in adults (11/26 cases). The edema usually clears rapidly with supportive care. Aggressive diagnostic and therapeutic interventions may be avoided if the syndrome is recognized. Maintenance of oxygenation and a patent airway are the mainstays of treatment. Pulmonary edema resulting from acute upper airway obstruction has been reported sporadically in children and adults since 1977.1Oswalt C.E. Gates G.A. Holmstrom F.M.G. Pulmonary edema as a complication of acute airway obstruction.JAMA. 1977; 238: 1833-1835Crossref PubMed Scopus (214) Google Scholar The predominant factor in its pathogenesis is the development of markedly negative intrathoracic and transpulmonary pressures by forced inspiration against a closed upper airway resulting in transudation of edema fluid from pulmonary capillaries into the interstitium.The true incidence of this type of pulmonary edema is uncertain, since many cases may have been missed and attributed to other causes because of a lack of familiarity with the syndrome. In a review of adult cases of upper airway obstruction requiring intubation or tracheostomy, 11 percent developed pulmonary edema.2Tami T.A. Chu F. Wildes T.O. Kaplan M. Pulmonary edema and acute upper airway obstruction.Laryngoscope. 1986; 96: 506-509Crossref PubMed Scopus (76) Google Scholar We present a case of postanesthetic laryngospasm-induced pulmonary edema in an adult and a review of the adult literature to highlight the need for recognition and appropriate treatment of this syndrome.CASE REPORTA previously healthy 28-year-old man with no known allergies was admitted for elective repair of an ankle fracture. Findings from his physical examination on admission were normal. Within minutes after extubation following successful surgery under general anesthesia, the patient developed respiratory distress with vigorous inspiratory efforts. Attempts at bag-mask ventilation revealed an obstructed airway, and a pulse oximeter showed desaturation to values below 50 percent. An initial dose of succinylcholine (25 mg intravenously) was given without success, but laryngospasm was promptly relieved after a second dose (100 mg intravenously). Despite high-flow oxygen by face mask, the oxygen saturation rose to only 83 percent. Examination of the chest showed diffuse rales and some wheezes, and the patient began coughing up copious amounts of frothy pink secretions. Nebulized metaproterenol and intravenous aminophylline were given.Subsequent examination by a pulmonary consultant revealed a muscular, alert man without a rash or jugular venous distention, but with a cough productive of pink frothy sputum. Blood pressure was 160/80 mm Hg, pulse rate was 110 beats per minute, and respiratory rate was 30/min. Diffuse bilateral rales were present without wheezes. No murmur or gallop was present. A chest roentgenogram (Fig 1) showed a pattern of pulmonary edema. Arterial blood gas levels with the patient receiving oxygen at 5L/min by face mask 15 minutes after the laryngospasm ended were pH of 7.37, arterial oxygen pressure (PaO2) of 62 mm Hg, and arterial carbon dioxide tension (PaCO2) of 51 mm Hg.Within an hour, the patient was comfortable, and coughing had subsided. Arterial blood gas levels with the patient breathing room air 18 hours after laryngospasm were pH of 7.39, PaO2 of 70 mm Hg, and PaCO2 of 47 mm Hg. The chest roentgenogram showed substantial clearing. Twenty-four hours later, with the patient breathing room air, the PaO2 was 83 mm Hg, the PaCO2 was 40 mm Hg, and the findings from chest examination were normal. The patient was discharged.REVIEW OF THE LITERATURETwenty-five cases of pulmonary edema due to upper airway obstruction in adults identified from the literature and the present case are listed in Table 1.1Oswalt C.E. Gates G.A. Holmstrom F.M.G. Pulmonary edema as a complication of acute airway obstruction.JAMA. 1977; 238: 1833-1835Crossref PubMed Scopus (214) Google Scholar, 2Tami T.A. Chu F. Wildes T.O. Kaplan M. Pulmonary edema and acute upper airway obstruction.Laryngoscope. 1986; 96: 506-509Crossref PubMed Scopus (76) Google Scholar, 3Rivera M. Hadlock F.P. O'Meara M.E. Pulmonary edema secondary to acute epiglottitis.Am J Roentgenol. 1979; 132: 991-992Crossref Scopus (11) Google Scholar, 4Jackson F.N. Rowland V. Corssen G. Laryngospasm-induced pulmonary edema.Chest. 1980; 78: 819-821Crossref PubMed Scopus (61) Google Scholar, 5Goldhill D.R. Dagleish J.G. Lake R.H.N. Respiratory problems and acromegaly.Anaesthesia. 1982; 37: 1200-1203Crossref PubMed Scopus (17) Google Scholar, 6Stradling J.R. Bolton P. Upper airway obstruction as a cause of pulmonary edema.Lancet. 1982; 1: 1353-1354Abstract PubMed Scopus (18) Google Scholar, 7Dash H.H. Cheriyan A.F. Singla R. Acute fulminating pulmonary edema following relief of airway obstruction.Indian J Chest Dis Allied Sci. 1983; 25: 145-148Google Scholar, 8Leatherman J.W. Schwartz S. Pulmonary edema due to upper airway obstruction.South Med J. 1983; 76: 1058-1060Crossref PubMed Scopus (17) Google Scholar, 9Jenkins J.G. Pulmonary edema following laryngospasm.Anesthesiology. 1984; 60: 611-612Crossref PubMed Scopus (13) Google Scholar, 10Melnick B.M. Postlaryngospasm pulmonary edema in adults.Anesthesiology. 1984; 60: 516-517Crossref PubMed Scopus (20) Google Scholar, 11Weisman C. Damask M.C. Yang J. Noncardiogenic pulmonary edema following laryngeal obstruction.Anesthesiology. 1984; 60: 163-165Crossref Scopus (44) Google Scholar, 12McGonagle M. Kennedy T.L. Laryngospasm induced pulmonary edema.Laryngoscope. 1984; 94: 1583-1585Crossref PubMed Scopus (21) Google Scholar, 13Batra R.K. Jayalaxmi T.S. Saksena R. Gode G.R. Acute pulmonary edema following an attempted suicidal hanging.Indian J Chest Dis Allied Sci. 1984; 26: 272-275PubMed Google Scholar, 14Glasser S.A. Siler J.N. Delayed onset of laryngospasm-induced pulmonary edema in an adult outpatient.Anesthesiology. 1985; 62: 370-371Crossref PubMed Scopus (40) Google Scholar, 15Lorch D.G. Sahn S.A. Post-extubation pulmonary edema following anesthesia induced by upper airway obstruction: are certain patients at increased risk?.Chest. 1986; 90: 802-805Crossref PubMed Scopus (90) Google Scholar, 16Stead W.W. Acute epiglottitis in adults.N Engl J Med. 1986; 315: 1163Crossref PubMed Scopus (7) Google Scholar, 17Randour P.H. Joucken K. Collard E. Mayne A. Pulmonary edema following acute upper airway obstruction.Acta Anaesthesiol Belg. 1986; 37: 225-231PubMed Google Scholar, 18Frank L.P. Schreiber G.C. Pulmonary edema following acute upper airway obstruction.Anesthesiology. 1986; 65: 106Crossref PubMed Scopus (26) Google Scholar, 19Lagler U. Russi E. Upper airway obstruction as a cause of pulmonary edema during late pregnancy.Am J Obstet Gynecol. 1987; 156: 643-644Abstract Full Text PDF PubMed Scopus (8) Google Scholar A similar number of male subjects (14) and female subjects (12) were affected. The median age was 40 years (range, 18 to 79 years). Most patients were free of diseases predisposing to pulmonary edema. The most common cause (11/26 or 42 percent) of upper airway obstruction was laryngospasm, with all but two cases occurring shortly after extubation.Table 1Published Reports of Pulmonary Edema Secondary to Acute Upper Airway Obstruction in AdultsReferenceAge (yr), SexObstructive EventAssociated ConditionsTime to OnsetTime to ResolutionMechanical VentilationHemodynamics*CVP, Central venous pressure; PAWP, pulmonary arterial wedge pressure; and PAP, pulmonary arterial pressure.Oswalt et al1Oswalt C.E. Gates G.A. Holmstrom F.M.G. Pulmonary edema as a complication of acute airway obstruction.JAMA. 1977; 238: 1833-1835Crossref PubMed Scopus (214) Google Scholar62,MLaryngeal tumorChronic obstructive pulmonary disease2.5 hr24 hNoCVP, 4 cm H2O26,FStrangulation…6 hr3 moYes…23,MHangingHypoxic brain injury30 min24 hYes…Rivera et al3Rivera M. Hadlock F.P. O'Meara M.E. Pulmonary edema secondary to acute epiglottitis.Am J Roentgenol. 1979; 132: 991-992Crossref Scopus (11) Google Scholar40,MEpiglottitis…On admission3 daysYesPAWP, 9 mm Hg; PAP, 24/14 mm HgJackson et al4Jackson F.N. Rowland V. Corssen G. Laryngospasm-induced pulmonary edema.Chest. 1980; 78: 819-821Crossref PubMed Scopus (61) Google Scholar33,FLaryngospasmObesity; short neck20 min24 hNo…Goldhill et al5Goldhill D.R. Dagleish J.G. Lake R.H.N. Respiratory problems and acromegaly.Anaesthesia. 1982; 37: 1200-1203Crossref PubMed Scopus (17) Google Scholar67,MAbnormal upper airway anatomy; postextubationAcromegalyMinutes24 hNo…Stradling et al6Stradling J.R. Bolton P. Upper airway obstruction as a cause of pulmonary edema.Lancet. 1982; 1: 1353-1354Abstract PubMed Scopus (18) Google Scholar35,FThyroid goiterPregnant 39 wkOn admission24 hYesPAWP, 12 mm Hg; PAP, 40/10 mm HgDash et al7Dash H.H. Cheriyan A.F. Singla R. Acute fulminating pulmonary edema following relief of airway obstruction.Indian J Chest Dis Allied Sci. 1983; 25: 145-148Google Scholar30,MTracheal tear; misplaced tracheal tubeAccidental strangulationImmediately after tube removed6 hYes…Leatherman and Schwartz8Leatherman J.W. Schwartz S. Pulmonary edema due to upper airway obstruction.South Med J. 1983; 76: 1058-1060Crossref PubMed Scopus (17) Google Scholar70,FThyroid tumor compressing trachea…On admission36 hPAWP, 7 mm HgJenkins9Jenkins J.G. Pulmonary edema following laryngospasm.Anesthesiology. 1984; 60: 611-612Crossref PubMed Scopus (13) Google Scholar60,FPostextubation laryngospasmTriple endoscopy; vocal cord stripping; difficult intubationWithin minutes24 hYes"Normal"Melnick10Melnick B.M. Postlaryngospasm pulmonary edema in adults.Anesthesiology. 1984; 60: 516-517Crossref PubMed Scopus (20) Google Scholar48,MPostextubation laryngospasmPossible obstructive sleep apnea30 sec24 hYes…21,FPostextubation laryngospasmNasal surgeryWithin minutes3 hNo…Weissman et al11Weisman C. Damask M.C. Yang J. Noncardiogenic pulmonary edema following laryngeal obstruction.Anesthesiology. 1984; 60: 163-165Crossref Scopus (44) Google Scholar46,MPostextubation laryngospasm…30 min24 hYesPAWP, 7 mm Hg;PAP, 30/17 mm HgMcGonagle and Kennedy12McGonagle M. Kennedy T.L. Laryngospasm induced pulmonary edema.Laryngoscope. 1984; 94: 1583-1585Crossref PubMed Scopus (21) Google Scholar20,MPostextubation laryngospasmNasal surgeryImmediately24 hYes…25,MPostextubation laryngospasm…Immediately18 hYes…Batra et al13Batra R.K. Jayalaxmi T.S. Saksena R. Gode G.R. Acute pulmonary edema following an attempted suicidal hanging.Indian J Chest Dis Allied Sci. 1984; 26: 272-275PubMed Google Scholar19,MHanging…On admission3 daysYes…Glasser and Siler14Glasser S.A. Siler J.N. Delayed onset of laryngospasm-induced pulmonary edema in an adult outpatient.Anesthesiology. 1985; 62: 370-371Crossref PubMed Scopus (40) Google Scholar30,FLaryngospasmGynecologic examination under mask anesthesia2 hr36 hNo…Lorchand Sahn15Lorch D.G. Sahn S.A. Post-extubation pulmonary edema following anesthesia induced by upper airway obstruction: are certain patients at increased risk?.Chest. 1986; 90: 802-805Crossref PubMed Scopus (90) Google Scholar48,MPostextubation laryngospasmTriple endoscopy; sleep apnea; obesity1 hr6 hNo…Stead16Stead W.W. Acute epiglottitis in adults.N Engl J Med. 1986; 315: 1163Crossref PubMed Scopus (7) Google Scholar46,MEpiglottitisImmediately…No…Tami et al2Tami T.A. Chu F. Wildes T.O. Kaplan M. Pulmonary edema and acute upper airway obstruction.Laryngoscope. 1986; 96: 506-509Crossref PubMed Scopus (76) Google Scholar45,FArytenoid edemaRheumatoid arthritis1 hr24 hYes…57,FSupraglottic cancerTracheostomyImmediately48 hYes…69,FLaryngeal polyp…Immediately48 hYes…Randour et al17Randour P.H. Joucken K. Collard E. Mayne A. Pulmonary edema following acute upper airway obstruction.Acta Anaesthesiol Belg. 1986; 37: 225-231PubMed Google Scholar79,MMalpositioned tracheal tube…Immediately48 hYesPAWP, 7 mm Hg; mean PAP, 20 mm HgFrank and Schreiber18Frank L.P. Schreiber G.C. Pulmonary edema following acute upper airway obstruction.Anesthesiology. 1986; 65: 106Crossref PubMed Scopus (26) Google Scholar38,FPostextubation laryngospasm…Immediately24 hYes…Lagler and Russi19Lagler U. Russi E. Upper airway obstruction as a cause of pulmonary edema during late pregnancy.Am J Obstet Gynecol. 1987; 156: 643-644Abstract Full Text PDF PubMed Scopus (8) Google Scholar35,FThyroid goiterPregnant 38 wkOn admission"Hours"Yes…Present case28,MPostextubation…Immediately24 hNo…* CVP, Central venous pressure; PAWP, pulmonary arterial wedge pressure; and PAP, pulmonary arterial pressure. Open table in a new tab In most cases, recognition of pulmonary edema occurred within minutes of relief of upper airway obstruction; however, in several cases, development of pulmonary edema was delayed for several hours. Because of this occasional delayed onset, it is recommended that patients who experience postanesthetic laryngospasm after outpatient surgery be observed for longer than the usual 60 to 90 minutes.14Glasser S.A. Siler J.N. Delayed onset of laryngospasm-induced pulmonary edema in an adult outpatient.Anesthesiology. 1985; 62: 370-371Crossref PubMed Scopus (40) Google Scholar Resolution of pulmonary edema occurred rapidly (within 48 hours) in all cases but one (after strangulation1Oswalt C.E. Gates G.A. Holmstrom F.M.G. Pulmonary edema as a complication of acute airway obstruction.JAMA. 1977; 238: 1833-1835Crossref PubMed Scopus (214) Google Scholar). All cases of laryngospasm-induced edema resolved in less than 36 hours.Treatment consisted of variable regimens of diuretics, digoxin, corticosteroids, morphine, and fluid restriction. A number of patients were managed with only supplemental oxygen and protection of the airway. Mechanical ventilation, frequently with the use of positive end-expiratory pressure (PEEP), was provided in 65 percent (17/26) of the whole series and in 55 percent (6/11) of those with laryngospasm. In six patients in whom hemodynamic measurements were made, the pulmonary arterial wedge pressure was normal and the pulmonary arterial pressure normal or slightly elevated. The rapid resolution of edema and the benign course followed by almost all of these patients suggest that a conservative approach to management may be indicated, with mechanical ventilation and PEEP reserved for those who cannot maintain adequate oxygenation while receiving oxygen by face mask.DISCUSSIONThe principal factor leading to pulmonary edema in upper airway obstruction appears to be the generation of markedly negative intrathoracic pressure due to forceful inspiratory effort against a closed upper airway resulting in a decrease in interstitial pressure favoring transudation of edema fluid from pulmonary capillaries.20Galvis A.G. Stool S.E. Bluestone C.D. Pulmonary edema following relief of acute upper airway obstruction.Ann Otol Rhinol Laryngol. 1980; 89: 124-128Crossref PubMed Scopus (84) Google Scholar Concomitant with the decreased interstitial pressure may be an increase in pulmonary blood flow due to increased venous return to the right side of the heart, further augmenting edema. Studies have demonstrated edema with inspiratory obstruction in animals21Haddy F.J. Campbell G.S. Visscher M.B. Pulmonary vascular pressures in relation to edema production by airway resistance and plethora in dogs.Am J Physiol. 1950; 161: 336-341PubMed Google Scholar and in a rabbit model of isolated perfused lung.22Smith-Erichsen N. Bø G. Airway closure and fluid filtration in the lung.Br J Anaesth. 1979; 51: 475-479Crossref PubMed Scopus (33) Google ScholarOther factors may play contributing roles in the development of edema with upper airway obstruction. Hypoxic vasoconstriction may increase capillary pressure and favor movement of fluid into the interstitium. The hyperadrenergic state associated with catastrophic airway obstruction can cause peripheral vasoconstriction and increased venous return to the right side of the heart, which could further increase pulmonary blood flow contributing to edema.Pulmonary edema usually occurs after relief of upper airway obstruction. It is postulated that upper airway obstruction creates more positive pressures during expiration which serves as a form of "auto-PEEP" to oppose transudation until the obstruction is removed. This idea has led to the recommendation of prophylactic continuous positive airway pressure, but the efficacy of this treatment has not been demonstrated.In summary, acute upper airway obstruction deserves greater recognition as a causative agent in pulmonary edema. Various causes of upper airway obstruction have resulted in a similar syndrome of rapid onset of pulmonary edema followed by quick resolution with supportive therapy. Aggressive hemodynamic monitoring, mechanical ventilation, or drug therapy is not needed in most cases. Maintenance of adequate oxygenation and a patent airway are the mainstays of management. Since postanesthetic laryngospasm is the most frequent cause of the syndrome in adults, those involved in postoperative care should be particularly aware of this syndrome. Pulmonary edema resulting from acute upper airway obstruction has been reported sporadically in children and adults since 1977.1Oswalt C.E. Gates G.A. Holmstrom F.M.G. Pulmonary edema as a complication of acute airway obstruction.JAMA. 1977; 238: 1833-1835Crossref PubMed Scopus (214) Google Scholar The predominant factor in its pathogenesis is the development of markedly negative intrathoracic and transpulmonary pressures by forced inspiration against a closed upper airway resulting in transudation of edema fluid from pulmonary capillaries into the interstitium. The true incidence of this type of pulmonary edema is uncertain, since many cases may have been missed and attributed to other causes because of a lack of familiarity with the syndrome. In a review of adult cases of upper airway obstruction requiring intubation or tracheostomy, 11 percent developed pulmonary edema.2Tami T.A. Chu F. Wildes T.O. Kaplan M. Pulmonary edema and acute upper airway obstruction.Laryngoscope. 1986; 96: 506-509Crossref PubMed Scopus (76) Google Scholar We present a case of postanesthetic laryngospasm-induced pulmonary edema in an adult and a review of the adult literature to highlight the need for recognition and appropriate treatment of this syndrome. CASE REPORTA previously healthy 28-year-old man with no known allergies was admitted for elective repair of an ankle fracture. Findings from his physical examination on admission were normal. Within minutes after extubation following successful surgery under general anesthesia, the patient developed respiratory distress with vigorous inspiratory efforts. Attempts at bag-mask ventilation revealed an obstructed airway, and a pulse oximeter showed desaturation to values below 50 percent. An initial dose of succinylcholine (25 mg intravenously) was given without success, but laryngospasm was promptly relieved after a second dose (100 mg intravenously). Despite high-flow oxygen by face mask, the oxygen saturation rose to only 83 percent. Examination of the chest showed diffuse rales and some wheezes, and the patient began coughing up copious amounts of frothy pink secretions. Nebulized metaproterenol and intravenous aminophylline were given.Subsequent examination by a pulmonary consultant revealed a muscular, alert man without a rash or jugular venous distention, but with a cough productive of pink frothy sputum. Blood pressure was 160/80 mm Hg, pulse rate was 110 beats per minute, and respiratory rate was 30/min. Diffuse bilateral rales were present without wheezes. No murmur or gallop was present. A chest roentgenogram (Fig 1) showed a pattern of pulmonary edema. Arterial blood gas levels with the patient receiving oxygen at 5L/min by face mask 15 minutes after the laryngospasm ended were pH of 7.37, arterial oxygen pressure (PaO2) of 62 mm Hg, and arterial carbon dioxide tension (PaCO2) of 51 mm Hg.Within an hour, the patient was comfortable, and coughing had subsided. Arterial blood gas levels with the patient breathing room air 18 hours after laryngospasm were pH of 7.39, PaO2 of 70 mm Hg, and PaCO2 of 47 mm Hg. The chest roentgenogram showed substantial clearing. Twenty-four hours later, with the patient breathing room air, the PaO2 was 83 mm Hg, the PaCO2 was 40 mm Hg, and the findings from chest examination were normal. The patient was discharged. A previously healthy 28-year-old man with no known allergies was admitted for elective repair of an ankle fracture. Findings from his physical examination on admission were normal. Within minutes after extubation following successful surgery under general anesthesia, the patient developed respiratory distress with vigorous inspiratory efforts. Attempts at bag-mask ventilation revealed an obstructed airway, and a pulse oximeter showed desaturation to values below 50 percent. An initial dose of succinylcholine (25 mg intravenously) was given without success, but laryngospasm was promptly relieved after a second dose (100 mg intravenously). Despite high-flow oxygen by face mask, the oxygen saturation rose to only 83 percent. Examination of the chest showed diffuse rales and some wheezes, and the patient began coughing up copious amounts of frothy pink secretions. Nebulized metaproterenol and intravenous aminophylline were given. Subsequent examination by a pulmonary consultant revealed a muscular, alert man without a rash or jugular venous distention, but with a cough productive of pink frothy sputum. Blood pressure was 160/80 mm Hg, pulse rate was 110 beats per minute, and respiratory rate was 30/min. Diffuse bilateral rales were present without wheezes. No murmur or gallop was present. A chest roentgenogram (Fig 1) showed a pattern of pulmonary edema. Arterial blood gas levels with the patient receiving oxygen at 5L/min by face mask 15 minutes after the laryngospasm ended were pH of 7.37, arterial oxygen pressure (PaO2) of 62 mm Hg, and arterial carbon dioxide tension (PaCO2) of 51 mm Hg. Within an hour, the patient was comfortable, and coughing had subsided. Arterial blood gas levels with the patient breathing room air 18 hours after laryngospasm were pH of 7.39, PaO2 of 70 mm Hg, and PaCO2 of 47 mm Hg. The chest roentgenogram showed substantial clearing. Twenty-four hours later, with the patient breathing room air, the PaO2 was 83 mm Hg, the PaCO2 was 40 mm Hg, and the findings from chest examination were normal. The patient was discharged. REVIEW OF THE LITERATURETwenty-five cases of pulmonary edema due to upper airway obstruction in adults identified from the literature and the present case are listed in Table 1.1Oswalt C.E. Gates G.A. Holmstrom F.M.G. Pulmonary edema as a complication of acute airway obstruction.JAMA. 1977; 238: 1833-1835Crossref PubMed Scopus (214) Google Scholar, 2Tami T.A. Chu F. Wildes T.O. Kaplan M. Pulmonary edema and acute upper airway obstruction.Laryngoscope. 1986; 96: 506-509Crossref PubMed Scopus (76) Google Scholar, 3Rivera M. Hadlock F.P. O'Meara M.E. Pulmonary edema secondary to acute epiglottitis.Am J Roentgenol. 1979; 132: 991-992Crossref Scopus (11) Google Scholar, 4Jackson F.N. Rowland V. Corssen G. Laryngospasm-induced pulmonary edema.Chest. 1980; 78: 819-821Crossref PubMed Scopus (61) Google Scholar, 5Goldhill D.R. Dagleish J.G. Lake R.H.N. Respiratory problems and acromegaly.Anaesthesia. 1982; 37: 1200-1203Crossref PubMed Scopus (17) Google Scholar, 6Stradling J.R. Bolton P. Upper airway obstruction as a cause of pulmonary edema.Lancet. 1982; 1: 1353-1354Abstract PubMed Scopus (18) Google Scholar, 7Dash H.H. Cheriyan A.F. Singla R. Acute fulminating pulmonary edema following relief of airway obstruction.Indian J Chest Dis Allied Sci. 1983; 25: 145-148Google Scholar, 8Leatherman J.W. Schwartz S. Pulmonary edema due to upper airway obstruction.South Med J. 1983; 76: 1058-1060Crossref PubMed Scopus (17) Google Scholar, 9Jenkins J.G. Pulmonary edema following laryngospasm.Anesthesiology. 1984; 60: 611-612Crossref PubMed Scopus (13) Google Scholar, 10Melnick B.M. Postlaryngospasm pulmonary edema in adults.Anesthesiology. 1984; 60: 516-517Crossref PubMed Scopus (20) Google Scholar, 11Weisman C. Damask M.C. Yang J. Noncardiogenic pulmonary edema following laryngeal obstruction.Anesthesiology. 1984; 60: 163-165Crossref Scopus (44) Google Scholar, 12McGonagle M. Kennedy T.L. Laryngospasm induced pulmonary edema.Laryngoscope. 1984; 94: 1583-1585Crossref PubMed Scopus (21) Google Scholar, 13Batra R.K. Jayalaxmi T.S. Saksena R. Gode G.R. Acute pulmonary edema following an attempted suicidal hanging.Indian J Chest Dis Allied Sci. 1984; 26: 272-275PubMed Google Scholar, 14Glasser S.A. Siler J.N. Delayed onset of laryngospasm-induced pulmonary edema in an adult outpatient.Anesthesiology. 1985; 62: 370-371Crossref PubMed Scopus (40) Google Scholar, 15Lorch D.G. Sahn S.A. Post-extubation pulmonary edema following anesthesia induced by upper airway obstruction: are certain patients at increased risk?.Chest. 1986; 90: 802-805Crossref PubMed Scopus (90) Google Scholar, 16Stead W.W. Acute epiglottitis in adults.N Engl J Med. 1986; 315: 1163Crossref PubMed Scopus (7) Google Scholar, 17Randour P.H. Joucken K. Collard E. Mayne A. Pulmonary edema following acute upper airway obstruction.Acta Anaesthesiol Belg. 1986; 37: 225-231PubMed Google Scholar, 18Frank L.P. Schreiber G.C. Pulmonary edema following acute upper airway obstruction.Anesthesiology. 1986; 65: 106Crossref PubMed Scopus (26) Google Scholar, 19Lagler U. Russi E. Upper airway obstruction as a cause of pulmonary edema during late pregnancy.Am J Obstet Gynecol. 1987; 156: 643-644Abstract Full Text PDF PubMed Scopus (8) Google Scholar A similar number of male subjects (14) and female subjects (12) were affected. The median age was 40 years (range, 18 to 79 years). Most patients were free of diseases predisposing to pulmonary edema. The most common cause (11/26 or 42 percent) of upper airway obstruction was laryngospasm, with all but two cases occurring shortly after extubation.Table 1Published Reports of Pulmonary Edema Secondary to Acute Upper Airway Obstruction in AdultsReferenceAge (yr), SexObstructive EventAssociated ConditionsTime to OnsetTime to ResolutionMechanical VentilationHemodynamics*CVP, Central venous pressure; PAWP, pulmonary arterial wedge pressure; and PAP, pulmonary arterial pressure.Oswalt et al1Oswalt C.E. Gates G.A. Holmstrom F.M.G. Pulmonary edema as a complication of acute airway obstruction.JAMA. 1977; 238: 1833-1835Crossref PubMed Scopus (214) Google Scholar62,MLaryngeal tumorChronic obstructive pulmonary disease2.5 hr24 hNoCVP, 4 cm H2O26,FStrangulation…6 hr3 moYes…23,MHangingHypoxic brain injury30 min24 hYes…Rivera et al3Rivera M. Hadlock F.P. O'Meara M.E. Pulmonary edema secondary to acute epiglottitis.Am J Roentgenol. 1979; 132: 991-992Crossref Scopus (11) Google Scholar40,MEpiglottitis…On admission3 daysYesPAWP, 9 mm Hg; PAP, 24/14 mm HgJackson et al4Jackson F.N. Rowland V. Corssen G. Laryngospasm-induced pulmonary edema.Chest. 1980; 78: 819-821Crossref PubMed Scopus (61) Google Scholar33,FLaryngospasmObesity; short neck20 min24 hNo…Goldhill et al5Goldhill D.R. Dagleish J.G. Lake R.H.N. Respiratory problems and acromegaly.Anaesthesia. 1982; 37: 1200-1203Crossref PubMed Scopus (17) Google Scholar67,MAbnormal upper airway anatomy; postextubationAcromegalyMinutes24 hNo…Stradling et al6Stradling J.R. Bolton P. Upper airway obstruction as a cause of pulmonary edema.Lancet. 1982; 1: 1353-1354Abstract PubMed Scopus (18) Google Scholar35,FThyroid goiterPregnant 39 wkOn admission24 hYesPAWP, 12 mm Hg; PAP, 40/10 mm HgDash et al7Dash H.H. Cheriyan A.F. Singla R. Acute fulminating pulmonary edema following relief of airway obstruction.Indian J Chest Dis Allied Sci. 1983; 25: 145-148Google Scholar30,MTracheal tear; misplaced tracheal tubeAccidental strangulationImmediately after tube removed6 hYes…Leatherman and Schwartz8Leatherman J.W. Schwartz S. Pulmonary edema due to upper airway obstruction.South Med J. 1983; 76: 1058-1060Crossref PubMed Scopus (17) Google Scholar70,FThyroid tumor compressing trachea…On admission36 hPAWP, 7 mm HgJenkins9Jenkins J.G. Pulmonary edema following laryngospasm.Anesthesiology. 1984; 60: 611-612Crossref PubMed Scopus (13) Google Scholar60,FPostextubation laryngospasmTriple endoscopy; vocal cord stripping; difficult intubationWithin minutes24 hYes"Normal"Melnick10Melnick B.M. Postlaryngospasm pulmonary edema in adults.Anesthesiology. 1984; 60: 516-517Crossref PubMed Scopus (20) Google Scholar48,MPostextubation laryngospasmPossible obstructive sleep apnea30 sec24 hYes…21,FPostextubation laryngospasmNasal surgeryWithin minutes3 hNo…Weissman et al11Weisman C. Damask M.C. Yang J. Noncardiogenic pulmonary edema following laryngeal obstruction.Anesthesiology. 1984; 60: 163-165Crossref Scopus (44) Google Scholar46,MPostextubation laryngospasm…30 min24 hYesPAWP, 7 mm Hg;PAP, 30/17 mm HgMcGonagle and Kennedy12McGonagle M. Kennedy T.L. Laryngospasm induced pulmonary edema.Laryngoscope. 1984; 94: 1583-1585Crossref PubMed Scopus (21) Google Scholar20,MPostextubation laryngospasmNasal surgeryImmediately24 hYes…25,MPostextubation laryngospasm…Immediately18 hYes…Batra et al13Batra R.K. Jayalaxmi T.S. Saksena R. Gode G.R. Acute pulmonary edema following an attempted suicidal hanging.Indian J Chest Dis Allied Sci. 1984; 26: 272-275PubMed Google Scholar19,MHanging…On admission3 daysYes…Glasser and Siler14Glasser S.A. Siler J.N. Delayed onset of laryngospasm-induced pulmonary edema in an adult outpatient.Anesthesiology. 1985; 62: 370-371Crossref PubMed Scopus (40) Google Scholar30,FLaryngospasmGynecologic examination under mask anesthesia2 hr36 hNo…Lorchand Sahn15Lorch D.G. Sahn S.A. Post-extubation pulmonary edema following anesthesia induced by upper airway obstruction: are certain patients at increased risk?.Chest. 1986; 90: 802-805Crossref PubMed Scopus (90) Google Scholar48,MPostextubation laryngospasmTriple endoscopy; sleep apnea; obesity1 hr6 hNo…Stead16Stead W.W. Acute epiglottitis in adults.N Engl J Med. 1986; 315: 1163Crossref PubMed Scopus (7) Google Scholar46,MEpiglottitisImmediately…No…Tami et al2Tami T.A. Chu F. Wildes T.O. Kaplan M. Pulmonary edema and acute upper airway obstruction.Laryngoscope. 1986; 96: 506-509Crossref PubMed Scopus (76) Google Scholar45,FArytenoid edemaRheumatoid arthritis1 hr24 hYes…57,FSupraglottic cancerTracheostomyImmediately48 hYes…69,FLaryngeal polyp…Immediately48 hYes…Randour et al17Randour P.H. Joucken K. Collard E. Mayne A. Pulmonary edema following acute upper airway obstruction.Acta Anaesthesiol Belg. 1986; 37: 225-231PubMed Google Scholar79,MMalpositioned tracheal tube…Immediately48 hYesPAWP, 7 mm Hg; mean PAP, 20 mm HgFrank and Schreiber18Frank L.P. Schreiber G.C. Pulmonary edema following acute upper airway obstruction.Anesthesiology. 1986; 65: 106Crossref PubMed Scopus (26) Google Scholar38,FPostextubation laryngospasm…Immediately24 hYes…Lagler and Russi19Lagler U. Russi E. Upper airway obstruction as a cause of pulmonary edema during late pregnancy.Am J Obstet Gynecol. 1987; 156: 643-644Abstract Full Text PDF PubMed Scopus (8) Google Scholar35,FThyroid goiterPregnant 38 wkOn admission"Hours"Yes…Present case28,MPostextubation…Immediately24 hNo…* CVP, Central venous pressure; PAWP, pulmonary arterial wedge pressure; and PAP, pulmonary arterial pressure. Open table in a new tab In most cases, recognition of pulmonary edema occurred within minutes of relief of upper airway obstruction; however, in several cases, development of pulmonary edema was delayed for several hours. Because of this occasional delayed onset, it is recommended that patients who experience postanesthetic laryngospasm after outpatient surgery be observed for longer than the usual 60 to 90 minutes.14Glasser S.A. Siler J.N. Delayed onset of laryngospasm-induced pulmonary edema in an adult outpatient.Anesthesiology. 1985; 62: 370-371Crossref PubMed Scopus (40) Google Scholar Resolution of pulmonary edema occurred rapidly (within 48 hours) in all cases but one (after strangulation1Oswalt C.E. Gates G.A. Holmstrom F.M.G. Pulmonary edema as a complication of acute airway obstruction.JAMA. 1977; 238: 1833-1835Crossref PubMed Scopus (214) Google Scholar). All cases of laryngospasm-induced edema resolved in less than 36 hours.Treatment consisted of variable regimens of diuretics, digoxin, corticosteroids, morphine, and fluid restriction. A number of patients were managed with only supplemental oxygen and protection of the airway. Mechanical ventilation, frequently with the use of positive end-expiratory pressure (PEEP), was provided in 65 percent (17/26) of the whole series and in 55 percent (6/11) of those with laryngospasm. In six patients in whom hemodynamic measurements were made, the pulmonary arterial wedge pressure was normal and the pulmonary arterial pressure normal or slightly elevated. The rapid resolution of edema and the benign course followed by almost all of these patients suggest that a conservative approach to management may be indicated, with mechanical ventilation and PEEP reserved for those who cannot maintain adequate oxygenation while receiving oxygen by face mask. Twenty-five cases of pulmonary edema due to upper airway obstruction in adults identified from the literature and the present case are listed in Table 1.1Oswalt C.E. Gates G.A. Holmstrom F.M.G. Pulmonary edema as a complication of acute airway obstruction.JAMA. 1977; 238: 1833-1835Crossref PubMed Scopus (214) Google Scholar, 2Tami T.A. Chu F. Wildes T.O. Kaplan M. Pulmonary edema and acute upper airway obstruction.Laryngoscope. 1986; 96: 506-509Crossref PubMed Scopus (76) Google Scholar, 3Rivera M. Hadlock F.P. O'Meara M.E. Pulmonary edema secondary to acute epiglottitis.Am J Roentgenol. 1979; 132: 991-992Crossref Scopus (11) Google Scholar, 4Jackson F.N. Rowland V. Corssen G. Laryngospasm-induced pulmonary edema.Chest. 1980; 78: 819-821Crossref PubMed Scopus (61) Google Scholar, 5Goldhill D.R. Dagleish J.G. Lake R.H.N. Respiratory problems and acromegaly.Anaesthesia. 1982; 37: 1200-1203Crossref PubMed Scopus (17) Google Scholar, 6Stradling J.R. Bolton P. Upper airway obstruction as a cause of pulmonary edema.Lancet. 1982; 1: 1353-1354Abstract PubMed Scopus (18) Google Scholar, 7Dash H.H. Cheriyan A.F. Singla R. Acute fulminating pulmonary edema following relief of airway obstruction.Indian J Chest Dis Allied Sci. 1983; 25: 145-148Google Scholar, 8Leatherman J.W. Schwartz S. Pulmonary edema due to upper airway obstruction.South Med J. 1983; 76: 1058-1060Crossref PubMed Scopus (17) Google Scholar, 9Jenkins J.G. Pulmonary edema following laryngospasm.Anesthesiology. 1984; 60: 611-612Crossref PubMed Scopus (13) Google Scholar, 10Melnick B.M. Postlaryngospasm pulmonary edema in adults.Anesthesiology. 1984; 60: 516-517Crossref PubMed Scopus (20) Google Scholar, 11Weisman C. Damask M.C. Yang J. Noncardiogenic pulmonary edema following laryngeal obstruction.Anesthesiology. 1984; 60: 163-165Crossref Scopus (44) Google Scholar, 12McGonagle M. Kennedy T.L. Laryngospasm induced pulmonary edema.Laryngoscope. 1984; 94: 1583-1585Crossref PubMed Scopus (21) Google Scholar, 13Batra R.K. Jayalaxmi T.S. Saksena R. Gode G.R. Acute pulmonary edema following an attempted suicidal hanging.Indian J Chest Dis Allied Sci. 1984; 26: 272-275PubMed Google Scholar, 14Glasser S.A. Siler J.N. Delayed onset of laryngospasm-induced pulmonary edema in an adult outpatient.Anesthesiology. 1985; 62: 370-371Crossref PubMed Scopus (40) Google Scholar, 15Lorch D.G. Sahn S.A. Post-extubation pulmonary edema following anesthesia induced by upper airway obstruction: are certain patients at increased risk?.Chest. 1986; 90: 802-805Crossref PubMed Scopus (90) Google Scholar, 16Stead W.W. Acute epiglottitis in adults.N Engl J Med. 1986; 315: 1163Crossref PubMed Scopus (7) Google Scholar, 17Randour P.H. Joucken K. Collard E. Mayne A. Pulmonary edema following acute upper airway obstruction.Acta Anaesthesiol Belg. 1986; 37: 225-231PubMed Google Scholar, 18Frank L.P. Schreiber G.C. Pulmonary edema following acute upper airway obstruction.Anesthesiology. 1986; 65: 106Crossref PubMed Scopus (26) Google Scholar, 19Lagler U. Russi E. Upper airway obstruction as a cause of pulmonary edema during late pregnancy.Am J Obstet Gynecol. 1987; 156: 643-644Abstract Full Text PDF PubMed Scopus (8) Google Scholar A similar number of male subjects (14) and female subjects (12) were affected. The median age was 40 years (range, 18 to 79 years). Most patients were free of diseases predisposing to pulmonary edema. The most common cause (11/26 or 42 percent) of upper airway obstruction was laryngospasm, with all but two cases occurring shortly after extubation. In most cases, recognition of pulmonary edema occurred within minutes of relief of upper airway obstruction; however, in several cases, development of pulmonary edema was delayed for several hours. Because of this occasional delayed onset, it is recommended that patients who experience postanesthetic laryngospasm after outpatient surgery be observed for longer than the usual 60 to 90 minutes.14Glasser S.A. Siler J.N. Delayed onset of laryngospasm-induced pulmonary edema in an adult outpatient.Anesthesiology. 1985; 62: 370-371Crossref PubMed Scopus (40) Google Scholar Resolution of pulmonary edema occurred rapidly (within 48 hours) in all cases but one (after strangulation1Oswalt C.E. Gates G.A. Holmstrom F.M.G. Pulmonary edema as a complication of acute airway obstruction.JAMA. 1977; 238: 1833-1835Crossref PubMed Scopus (214) Google Scholar). All cases of laryngospasm-induced edema resolved in less than 36 hours. Treatment consisted of variable regimens of diuretics, digoxin, corticosteroids, morphine, and fluid restriction. A number of patients were managed with only supplemental oxygen and protection of the airway. Mechanical ventilation, frequently with the use of positive end-expiratory pressure (PEEP), was provided in 65 percent (17/26) of the whole series and in 55 percent (6/11) of those with laryngospasm. In six patients in whom hemodynamic measurements were made, the pulmonary arterial wedge pressure was normal and the pulmonary arterial pressure normal or slightly elevated. The rapid resolution of edema and the benign course followed by almost all of these patients suggest that a conservative approach to management may be indicated, with mechanical ventilation and PEEP reserved for those who cannot maintain adequate oxygenation while receiving oxygen by face mask. DISCUSSIONThe principal factor leading to pulmonary edema in upper airway obstruction appears to be the generation of markedly negative intrathoracic pressure due to forceful inspiratory effort against a closed upper airway resulting in a decrease in interstitial pressure favoring transudation of edema fluid from pulmonary capillaries.20Galvis A.G. Stool S.E. Bluestone C.D. Pulmonary edema following relief of acute upper airway obstruction.Ann Otol Rhinol Laryngol. 1980; 89: 124-128Crossref PubMed Scopus (84) Google Scholar Concomitant with the decreased interstitial pressure may be an increase in pulmonary blood flow due to increased venous return to the right side of the heart, further augmenting edema. Studies have demonstrated edema with inspiratory obstruction in animals21Haddy F.J. Campbell G.S. Visscher M.B. Pulmonary vascular pressures in relation to edema production by airway resistance and plethora in dogs.Am J Physiol. 1950; 161: 336-341PubMed Google Scholar and in a rabbit model of isolated perfused lung.22Smith-Erichsen N. Bø G. Airway closure and fluid filtration in the lung.Br J Anaesth. 1979; 51: 475-479Crossref PubMed Scopus (33) Google ScholarOther factors may play contributing roles in the development of edema with upper airway obstruction. Hypoxic vasoconstriction may increase capillary pressure and favor movement of fluid into the interstitium. The hyperadrenergic state associated with catastrophic airway obstruction can cause peripheral vasoconstriction and increased venous return to the right side of the heart, which could further increase pulmonary blood flow contributing to edema.Pulmonary edema usually occurs after relief of upper airway obstruction. It is postulated that upper airway obstruction creates more positive pressures during expiration which serves as a form of "auto-PEEP" to oppose transudation until the obstruction is removed. This idea has led to the recommendation of prophylactic continuous positive airway pressure, but the efficacy of this treatment has not been demonstrated.In summary, acute upper airway obstruction deserves greater recognition as a causative agent in pulmonary edema. Various causes of upper airway obstruction have resulted in a similar syndrome of rapid onset of pulmonary edema followed by quick resolution with supportive therapy. Aggressive hemodynamic monitoring, mechanical ventilation, or drug therapy is not needed in most cases. Maintenance of adequate oxygenation and a patent airway are the mainstays of management. Since postanesthetic laryngospasm is the most frequent cause of the syndrome in adults, those involved in postoperative care should be particularly aware of this syndrome. The principal factor leading to pulmonary edema in upper airway obstruction appears to be the generation of markedly negative intrathoracic pressure due to forceful inspiratory effort against a closed upper airway resulting in a decrease in interstitial pressure favoring transudation of edema fluid from pulmonary capillaries.20Galvis A.G. Stool S.E. Bluestone C.D. Pulmonary edema following relief of acute upper airway obstruction.Ann Otol Rhinol Laryngol. 1980; 89: 124-128Crossref PubMed Scopus (84) Google Scholar Concomitant with the decreased interstitial pressure may be an increase in pulmonary blood flow due to increased venous return to the right side of the heart, further augmenting edema. Studies have demonstrated edema with inspiratory obstruction in animals21Haddy F.J. Campbell G.S. Visscher M.B. Pulmonary vascular pressures in relation to edema production by airway resistance and plethora in dogs.Am J Physiol. 1950; 161: 336-341PubMed Google Scholar and in a rabbit model of isolated perfused lung.22Smith-Erichsen N. Bø G. Airway closure and fluid filtration in the lung.Br J Anaesth. 1979; 51: 475-479Crossref PubMed Scopus (33) Google Scholar Other factors may play contributing roles in the development of edema with upper airway obstruction. Hypoxic vasoconstriction may increase capillary pressure and favor movement of fluid into the interstitium. The hyperadrenergic state associated with catastrophic airway obstruction can cause peripheral vasoconstriction and increased venous return to the right side of the heart, which could further increase pulmonary blood flow contributing to edema. Pulmonary edema usually occurs after relief of upper airway obstruction. It is postulated that upper airway obstruction creates more positive pressures during expiration which serves as a form of "auto-PEEP" to oppose transudation until the obstruction is removed. This idea has led to the recommendation of prophylactic continuous positive airway pressure, but the efficacy of this treatment has not been demonstrated. In summary, acute upper airway obstruction deserves greater recognition as a causative agent in pulmonary edema. Various causes of upper airway obstruction have resulted in a similar syndrome of rapid onset of pulmonary edema followed by quick resolution with supportive therapy. Aggressive hemodynamic monitoring, mechanical ventilation, or drug therapy is not needed in most cases. Maintenance of adequate oxygenation and a patent airway are the mainstays of management. Since postanesthetic laryngospasm is the most frequent cause of the syndrome in adults, those involved in postoperative care should be particularly aware of this syndrome.
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