CORRESPONDENCE 213 nized and the patient returned to an ED, 14 hours after being discharged from same-day surgery for hemorrhoidectomy, in florid pulmonary edema requiring emergent intubation and 3 days of ventilator support. 6 There are many theories on the mechanism for APOPE. 1,2,6 Recently, its causality has been split into two types. Type 1 follows acute airway obstruction such as laryngospasm, spasmodic croup, or epiglottitis. The patient inspires against the acute obstruction, which leads to a decrease in intrathoracic pressure followed by an increase in venous return. The elevated amounts of lung blood volume produce an increase in hydrostatic pressure and pulmonary vessel distension. Transudation from the capillary bed to the interstitium induces blood-tinged type 1 APOPE. 7 Type 2 occurs after relief of chronic upper airway obstruction such as tonsil and adenoid hypertrophy. When there is an obstruc- tion over an extended period of time, an intrinsic PEEP develops. This produces a higher intrathoracic pressure that compensates for the lower pressures on inspiration. 5 Hence, when a chronic obstruction is relieved, there is a sudden decrease in intrathoracic pressures and a subsequent increase in venous return and pulmonary blood volume. This makes it more likely that transudation will occur from the vascular bed to the interstitium, resulting in type 2 APOPE. 7 In our patient, it is not clear if this is type 1 or type 2. We did not attain a preintubation film, and the lungs were difficult to auscultate because of stridor. There are case reports that include chest X-rays before and after intubation of an acute upper airway obstruction, with the preintubation film being normal and the postintubation film showing florid pulmonary edema, s Classic findings on antero- posterior portable chest radiographs indicative for APOPE are bilateral centralized pulmonary edema, a wide vascular pedicle, and a normal cardiothoracic ratio. 9 Treatment of postobstructive pulmonary edema is supportive and includes maintenance of airway patency, oxygen supplementa- tion, diuresis, and maintenance of PEER 10 Intravenous crystalloids should be restricted, and colloids may be used] Pulmonary edema develops within 90 minutes of laryngospasm resolution (usually instantly) and in 70% of patients resolves within 24 hours. Mechanical ventilation when required is withdrawn from 40% of patients within 12 hours. PEEP (5 to 20 cm of water) has been used in all patients requiring ventilator support. Furosemide is the most frequently used pharmacotherapy, in half the patients, u Other medica- tions used are digoxin, steroids, morphine, and theophylline, yet their efficacy has not been proven. 12 The use of intravenous lidocaine (1.5 to 2 mg/kg) prior to intubation is also advocated--it has been shown to reduce the incidence of laryngospasm. 2 Emergency physicians should be aware of acute pulmonary edema as a complication of intubating an edematous, obstructed airway and should treat this phenomenon with oxygen, PEER and diuresis. APOPE also occurs in young healthy adults who undergo same-day surgery. Hypoxic, tachypneic adults or children who present to the ED after recently being extubated should have APOPE included in their differential diagnosis. GARYFALLOS T. GARYFALLOU, MD The Emergency Department St. Joseph's Hospital Denver, CO STEVENK. COSTALAS, DO CHRISTOPHER J. MURPHY,MD Department of Emergency Medicine Medical Center of Delaware Newark, DE References 1. Bonadio WA, Losek JD: The characteristics of children with epiglottitis who develop the complication of pulmonary edema. Arch Otolaryngol Head Neck Surg 1991 ;117:205-207 2. Wilson GW, Bircher NC: Acute pulmonary edema developing after laryngospasm: Report of a case. J Oral Maxillofac Surg 1995;53:211-214 3. Oswalt CE, Gates GA, Holstrom FMG: Pulmonary edema as a complication of acute upper airway obstruction. JAMA 1977;238:1833- 1835 4. Travis DW, Todres ID, Shannon DC: Pulmonary edema associ- ated with croup and epiglottitis. Pediatrics 1977;59:695-698 5. Galvis A, Stool SE, Bluestone CD: Pulmonary edema following relief of acute upper airway obstruction. Ann Oto11980;899:124-128 6. Holmes JR, Hensinger RN, Wojtys EW: Postoperative pulmo- nary edema in young, athletic adults. Am J Sports Med 1991;19:365- 371 7. Guffin TN, Har-EI G, Sanders A, et al: Acute postobstructive pulmonary edema. Otolaryngol Head Neck Surg 1995;112:235-237 8. Oudjhane K, Bowen A, Oh KS, et al: Pulmonary edema complicating upper airway obstruction in infants and children. Can Assoc Radiol J 1992;43:278-282 9. Cascade PN, Alexander GD, Mackie DS: Negative-pressure pulmonary edema after endotracheal intubation. Radiology 1993;186: 671-675 10. Wiesel S, Gutman JBL, Kleiman SJ: Adult epiglottitis and postobstructive pulmonary edema in a patient with severe coronary artery disease. J Clin Anesth 1993;5:158-162 11. Harlow KD, Ford EG: Pulmonary edema following post- operative laryngospasm: A case report and review of the literature. Am Surgeon 1993;59:443-447 12. Goitz R J, Goitz HT, Difazio CA, et al: Identification of acute pulmonary edema following routine outpatient orthopedic procedures in healthy young athletes. Orthopedics 1994;17:949-952 MISSILE EMBOLITO THE PULMONARY ARTERY To the Editor:--Despite the large number of gunshot wounds treated in civilian practice, embolization of missiles to the pulmo- nary artery is uncommon. 1-4 A review of 7,500 medical reports from casualties of the Vietnam War revealed 22 missile emboli, only 4 of which were to the pulmonary artery. 5 Missile emboli to the pulmonary artery provide a diagnostic challenge and a therapeu- tic dilemma. We report a case of a missile embolus to the pulmonary artery, diagnostic difficulties, and review of the fiterature. A 41-year-old patient was brought to the emergency department with two separate bullet wounds. No exit wounds were identified. This case was referred to the radiology department for localization of the bullets. Abdominal X-ray showed one bullet lying in the fight iliac fossa. X-ray of the chest showed a second bullet located in the region of the right ventricle (Figure 1). Exploratory thoracotomy was done, but no bullet was found in the ventricles or pericardium. Subsequent computed tomography (CT) of the chest showed that the bullet had migrated to the right lower lobe pulmonary artery, resulting in infarction of the fight posterior basal segment (Figure 2). The patient was managed conservatively and no attempt was made to remove this bullet. Repeat CT 3 weeks later showed partial resolution of the pulmonary infarct and no further migration of the missile was noted. The patient was subsequently discharged without cardiopulmonary complaints. Most patients with missile emboli are asymptomatic. 6 Com- plaints of chest pain, dyspnea, and hemoptysis in patients with missile emboli are related to chest wall injury and hypotension from blood loss and not from embolism per se. 7-9 This lack of symptomatology may result in delay in diagnosis. Low-velocity and small-caliber missiles have a greater tendency to embolize through injury to a large vein or the right heart chambers. The migration of the bullet most likely results from body position, respiratory motion, blood flow, and gravitational forces. 6,9,1° The