Pulmonary Edema due to Upper Airway Obstruction in Adults

Osiers node , which responded well to a short course of indomethacin. It is very possible that the pain was caused by an inflammatory reaction in the Osiers node. ACKXO\VLEDG~IEXT:

photographs.

I thank

~Ir.

John Randall for taking the

REFEREXCES

2 3 4 5

Scheid ~A , Sande ~1A. Endocarditis and intravascular infections. In: Mandell GL , Douglas RG Jr, Bennett JE , eds. Principles and practice of infectious diseases. 2nd ed . Xew York: John Wiley & Sons, 1985:504-30 Puklin JE, Balis GA, Bentley OW Culture of an Osiers node . Arch Intern Med 1971; 127:296-98 Alpert JS, Krous HF, Dalen JE, O'Rourke RA, Bloor CM . Pathogenesis of Osiers nodes . Ann Intern Med 1976; 85:471-73 YeeJ, ~lcAllister CK . The utilit y of Osiers nodes in the diagnosis of infective endocarditis. Chest 1987; 92:751-52 Kerr A Jr. Subacute bacterial endocarditis. Springfield , Ill: Charles C Thomas, 1955:105

Pulmonary Edema due to Upper Airway Obstruction in Adults· Docid Willms, .\1.D .;t and Deborah Shure , M.D . , F .C .C .P.~ 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. (Chest 1988;

percent developed pulmonary edema.' 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 REPORT

A previously healthy 28-year-old man with no known allergies was admitted for elective repair of an ankle fracture . Findings from his ph ysical 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 3O/min. Diffuse bilateral rales were present without wheezes. Xo murmur or gallop was present. A chest roentgenogram (Fig 1) showed a pattern of pulmonary edema. Arte rial blood gas levels with the patient receiving oxygen at 5Umin by face mask 15 minutes after the laryngospasm ended were pH of 7.37, arterial oxygen pre ssure (PaO,) of 62 mm Hg, and arterial carbon dioxide tension (PaCO,) of 51 mm Hg. Within an hour, the patient was comfortable, and coughing had subs ided. Arterial blood gas levels with the patient breathing room air 18 hours after laryngospasm were pH of 7.39, PaO, of 70 mm Hg, and PaCO, of 47 mm Hg. The chest roentgenogram showed substantial clearing. Twenty-four hours later, with the patient breathing room air, the PaO, was 83 mm Hg, the PaCO, was 40 mm Hg, and the findings from chest examination were normal . The

94:1090-92)

P

u lm on ar y edema resulting from acute upper airway obstruction has been reported sporadically in children and adults since 1977.' 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 ·From the Division of Pulmonary and Critical Care Medicine, University of Californ ia, San Diego. tPulmonary Fellow. 1:AssociateProfessor of Medicine, and Chief, Division of Pulmonary and Critical Care Medicine, Veterans Administration Medical Center, San Diego . Reprint requests : Dr. Willms, 225 Dickinson Street, H-772, San Diego 92103 1090

FIGURE

spasm .

1. Chest roentgenogram minutes after relief of laryngo-

Pulmonary Edema due to Upper Airway Obstruction (Willms, Shure)

Table l-PubU,hed Reports ofPulmoraary Edema Secondary to Acute Upper AinDGY Ob.truction in Adults

Reference

Age (yr1 Sex

Obstructive Event

Oswalt et all

62,M

Laryngeal tumor

Rivera et al3

26,F 23,M 4O,M

Strangulation Hanging Epiglottitis

Jackson et al4 Goldhi11 et al5

33,F 67,M

Stradling

35,F

et al6

Laryngospasm Abnormal upper airway anatomy; postextubation Thyroid goiter

3O,M

Tracheal tear; misplaced tracheal tube

Leatherman and Schwartzi Jenkins8

70,F 6O,F

Thyroid tumor compressing trachea Postextubation laryngospasm

Melnick'?

48,M 21,F

Weissman et al11

46,M

McGonagle and KennedylJ

20,M 25,M

Randour et al17

19,M 3O,F 48,M 46,M 45,F 57,F 69,F 79,M

Postextubation laryngospasm Postextubation laryngospasm Postextubation laryngospasm Postextubation laryngospasm Postextubation laryngospasm Hanging Laryngospasm Postextubation laryngospasm Epiglottitis Arytenoid edema Supraglottic cancer Laryngeal polyp Malpositioned tracheal tube

Frank and

38,F

Lagler and Russi 18 Present case

35,F

Postextubation laryngospasm Thyroid goiter

28,M

Postextubation

Schreiber"

.CV~

Chronic obstructive pulmonary disease Hypoxic brain injury

Time to Onset

Time to Resolution

Hemodynamics"

2.5hr

24h

No

C~4cmH10

6hr 30 min On admission

3mo 24h 3 days

Yes Yes Yes

PA~9mmHg;

Obesity; short neck Acromegaly

20 min Minutes

24h 24h

No No

Pregnant 39 wk

On admission

24h

Yes

PA~ 24/14 mmHg

I2mmHg; 40/10 mmHg

PA~

P~

Dash et al7

Batra et al13 Glasser and Siler14 Lorch and Sahn 15 Stead16 'Iami et all

Associated Conditions

Mechanieal Ventilation

Accidental strangulation

'Iriple endoscopy; vocal cord stripping; difBcult intubation Possible obstructive sleep apnea Nasal surgery

Immediately after tube removed On admission

6h

Yes

36h

PAW~

.Within minutes

24h

Yes

30 sec

24h

Yes

3h

No

24h

Yes

Within minutes 30 min

"Normal"

PA~7mmHg;

PA~

Nasal surgery

Gynecologic examination under mask anesthesia mple endoscopy; sleep apnea; obesity Rheumatoid arthritis 'fracheostomy

Immediately

24h

Yes

Immediately

ISh

Yes

On admission 2hr

3 days 36h

Yes No

Ihr Immediately

Ihr

Immediately Immediately Immediately

6h

No

24h 48h 48h 48h

No Yes Yes Yes Yes

7mmHg

30117

mmHg

PA~7mmHg;

meanP~

Pregnant 38 wk

Immediately

24h

Yes

On admission

"Hours"

Yes

Immediately

24h

No

20mmHg

Central venous pressure; PAW~ pulmonary arterial wedge pressure; and P~ pulmonary arterial pressure.

patient was discharged. REVIEW OF THE LITERATURE

1\venty-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. 1-18 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 CHEST I 94 I 5 I NOVEMBER, 1988

1081

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." Resolution of pulmonary edema occurred rapidly (within 48 hours) in all cases but one (after strangulation'), All cases of laryngospasm-induced edema resolved in less than 36 hours. 'Ireatment 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 (6111) 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. DISCUSSION

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. 20 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 animals" and in a rabbit model of isolated perfused lung. 21 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 1012

the most frequent cause of the syndrome in adults, those involved in postoperative care should be particularly aware of this syndrome. REFERENCES

1 Oswalt CE, Gates GA, Holmstrom FMG. Pulmonary edema as a complication of acute airway obstruction. JAMA 1977; 238:183335 2 'Iami TA, Chu F, Wildes TO, Kaplan M. Pulmonary edema and acute upper airway obstruction. Laryngoscope 1986; 96:506-09 3 Rivera M, Hadlock F~ O'Meara ME. Pulmonary edema secondary to acute epiglottitis. Am J Roentgenol1979; 132:991-92 4 Jackson FN, Rowland ~ Corssen G. Laryngospasm-induced pulmonary edema. Chest 1980; 78:819-21 5 Goldhill DR, Dagleish JG, Lake RHN. Respiratory problems and acromegaly Anaesthesia 1982; 37:1200-03 6 Stradling JR, Bolton E Upper airway obstruction as a cause of pulmonary edema. Lancet 1982; 1:1353-54 7 Dash HH, Cheriyan AF, Singla R. Acute fulminating pulmonary edema following relief of airway obstruction. Indian J Chest Dis Allied Sci 1983; 25:145-48 8 Leatherman M Schwartz S. Pulmonary edema due to upper airway obstruction. South Med J 1983; 76:1058-60 9 Jenkins JG. Pulmonary edema following laryngospasm. Anesthesiology 1984; 60:611-12 10 Melnick BM. Postlaryngospasm pulmonary edema in adults. Anesthesiology 1984; 60:516-17 11 ~isman C, Damask MC, Yang J. Noncardiogenic pulmonary edema following laryngeal obstruction. Anesthesiology 1984; 60:163-65 12 McGonagle M, Kennedy TL. Laryngospasm induced pulmonary edema. Laryngoscope 1984; 94:1583-85 13 Batra RIC, Jayalaxmi TS, Saksena R, Code GR. Acute pulmonary edema following an attempted suicidal hanging. Indian J Chest Dis Allied Sci 1984; 26:272-75 14 Glasser SA, Siler IN. Delayed onset of laryngospasm-induced pulmonary edema in an adult outpatient Anesthesiology 1985; 62:370-71 15 Lorch DG, Sahn SA. Post-extubation pulmonary edema following anesthesia induced by upper airway obstruction: are certain patients at increased risk? Chest 1986; 90:802-05 16 Stead ww. Acute epiglottitis in adults. N Engl J Med 1986; 315:1163 17 Randour PH, Joucken K, Collard E, Mayne A. Pulmonary edema following acute upper airway obstruction. Acta Anaesthesiol Belg 1986; 37:225-31 18 Frank ~ Schreiber GC. Pulmonary edema following acute upper airway obstruction. Anesthesiology 1986; 65:106 19 Lagler U, Russi E. Upper airway obstruction as a cause of pulmonary edema during late pregnancy Am J Obstet Gynecol 1987; 156:643-44 20 GalvisAG, StooISE, Bluestone CD. Pulmonary edema following relief of acute upper airway obstruction. Ann Otol Rhinol Laryngo1198O; 89:124-28 21 Haddy FJ, Campbell GS, Visscher MB. Pulmonary vascular pressures in relation to edema production by airway resistance and plethora in dogs. Am J Physioll950; 161:336-41 22 Smith-Erichsen N, 8fj G. Airway closure and fluid fUtration in the lung. Br J Anaesth 1979; 51:475-79 PulmonaryEdema due to Upper AJrway Obstruction (WIlms. Shute)