Pulmonarv Acute Su
Edema lottic Edema
Hiroshi Morisaki, MD,* Ryoichi Ochiai, MD,? Junzo Takeda, MD,+ Masao Nagano, MD8 Department
School of Medicine,
Presented here Zsa case of unilateral pulmonary edema following acute subglottic edema after removal of an endotracheal tube. A j-year-old boy, diagnosed as having nondiphtheric croup and pectus excavatum deformity, was scheduled for repair of a cleft lip. No complication occurred during the operation. After removal of the endotracheal tube, he showed dyspnea and cyanosis and was laterfound to have acute subglottic edema. After reintubation of the trachea, frothy pink fluid was discharged from the tube, and chest roentgenogram showed a right-sided alveolar infiltrate. Many factors may cause unilateral pulmonary edema, but it is suggested that acute subglottic edema and unilateral bronchial fragility strongly affected this episode.
Staff $Assistant Professor and Chairman
Address reprint requests to Dr. Morisaki at the Department of Anesthesiology, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160, Japan. Received for publication December 19, 1988; revised manuscript accepted for publication May 12, 1989. 0 1990 Butterworth
Introduction Bilateral pulmonary edema can occur as a complication of subacute upper airway obstruction.*mg Unilateral pulmonary edema, however, has not been reported as a complication of an upper airway obstruction such as subglottic edema. In this case, the child developed severe unilateral pulmonary edema following subglottic edema after removal of an endotracheal tube.
Keywords: Anesthesia, pediatric, extubation; airway, subglottic edema; complications, unilateral pulmonary edema.
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A 3-year-old boy weighing 17 kg was admitted for elective repair of a cleft lip. The boy was born at 41 weeks’ gestation, and birth weight was 3,680 g. At age 1 year 6 months, he was admitted to the hospital for 2 weeks because of respiratory distress due to nondiphtheric croup and asthmatic bronchitis. Then the patient developed severe pectus excavatum deformity. Owing to his large size for his age and macrocephalus without hydrocephalus, Sotos syndrome (cerebral gigantism syndrome) was suspected preoperatively. Since his pectus deformity was severe, chest roentgenogram showed cardiac enlargement on the posterior-anterior (PA) view and electrocardiogram
Unilateral pulmona~ edema after extubation: Morisaki et al.
(EKG) showed left ventricular hypertrophy, but there were no abnormal cardiorespiratory manifestations. Bromazepam 1.5 mg and atropine sulfate 0.3 mg were given as premeditation 1 hour before surgery. General anesthesia was induced with inhalation of 70% nitrous oxide and halothane. Following intravenous (IV) administration of succinylcholine chloride, endotracheal intubation (5.0 mm ID) was performed, and the tube was fixed at 15 cm from the tube tip at the front teeth. Air leakage around the tube during inflation was ascertained, and bilateral lung auscultation was normal. Before the incision, the surgeon packed the region of the epiglottis with gauze to prevent aspiration of blood during the operation. Anesthesia was maintained with 70% nitrous oxide and 0.75% to 1.0% halothane under controlled ventilation. There were no complications during the P-hour operation. The endotracheal tube was removed when the patient emerged from general anesthesia. A few minutes later, the patient developed severe intercostal and sternal retraction and cyanosis, which was not relieved by jaw lift or administration of 100% oxygen via mask. Endotracheal reintubation was attempted with a tube of the same size, but reintubation was impossible due to airway stenosis just below the vocal cord. Finally, an endotracheal tube of 3.0 mm ID was inserted with difficulty. Since the vocal cords appeared almost normal, dyspnea seemed most likely to be the result of subglottic edema. The patient’s vigorous motion resulted in accidental extubation. He became cyanotic again, and severe bradycardia (40 to 50 beats/minute) persisted for a few minutes. At this time, a tube of 4.0 mm ID was inserted, and a considerable amount of frothy pink fluid was discharged from the tube. Arterial blood gas analysis under high positive pressure ventilation with pure oxygen was as follows: pH, 6.92; PaCOt, 88 mmHg; PaO,, 424 mmHg; and baseexcess (BE), - 17. Chest roentgenogram showed a right-sided alveolar infiltrate (Figure I). Two hours after this episode, the patient was transported to the pediatric intensive-care unit. He was mechanically ventilated with an inspiratory oxygen fraction (FIO,) of 1.0, 10 cmH,O of positive endexpiratory pressure (PEEP), and an intermittent mandatory ventilation (IMV) rate of 30/minute. Arterial blood gas data were as follows: pH, 7.46; PaCO,, 27 mmHg; PaO,, 431 mmHg; BE, - 1.7. Six hours later, his blood gas data improved: pH, 7.44; PaCO,, 37 mmHg; PaO,, 123 mmHg; BE, 0.9 (FIO,, 0.4; PEEP, 6 cmH,O; IMV, 25/minute). Air leakage around the tube was not audible even at 30 cmH,O of inflation pressure. Dexamethasone 4 mg was administered for the subglottic edema.
Figure 1. Postoperative chest radiograph demonstrates severe right unilateral pulmonary edema.
Haziness of the right lung still remained on the chest radiograph the next morning. Two days after the episode, air leakage around the tube was detected at 12 cmH,O of airway pressure. Echocardiogram showed slightly decreased left ventricular contraction. Bronchoscopy via the endotracheal tube demonstrated that the right main stem bronchus became narrow during vigorous inspiration, but it was almost normal under the patient’s well-sedated condition the following day. The endotracheal tube was removed on the seventh day without further problems. Pulmonary ventilation/perfusion scan with Kr8 1m and Tc-99mMMA was normal. The boy was discharged from the hospital on the twenty-first postoperative day without any apparent sequelae.
Discussion Pulmonary edema following upper airway obstruction develops after the relief of extreme negative pressure in the airway, thus overcoming capillary hydrostatic pressure and lymphatic drainage.3,4 Furthermore, hypoxia causes massive sympathetic discharge, resulting in systemic vasoconstriction and a shift of blood from the systemic circulation to the low-resistance pulmoJ. Clin. Anesth., vol. 2, JadFeb
nary circulation. 5,6 Such mechanisms, however, usually result in bilateral pulmonary edema. In this case, pulmonary edema was unilateral. Accidental endobronchial intubation during an operation may later cause massive atelectasis and reexpansion pulmonary edema. This situation did not develop in the patient described here, since the depth of the endotracheal tube was known and auscultation of both lungs was normal. Calenoff et al.’ and other author&I3 have demonstrated several clinical conditions associated with unilateral pulmonary edema: systemic-to-pulmonary artery shunts with congenital heart disease, bronchial obstruction, unilateral venoocclusive disease, prolonged lateral decubitus position, unilateral aspiration, pulmonary contusion, unilateral infusion of hypotonic saline via a catheter misplaced in the pulmonary artery, and rapid thoracocentesis of pleural fluid and air. However, in this case, bronchoscopy and normal pulmonary scan showed that transient right bronchial obstruction was the primary reason for this episode rather than a pulmonary circulatory disturbance or other cause. The patient’s history of nondiphtheric croup and pectus excavatum deformity suggests the presence of tracheobronchomalacia or tracheobronchial fragility. The trachea and the proximal part of the main stem bronchi are located in extrapleural spaces. Given that the extrapleural right main stem bronchus may have been more fragile than normal, it could be easily collapsed during vigorous inspiratory efforts against acute subglottic edema, resulting in considerable negative pressure in the alveoli. In fact, bronchoscopy did show right main stem bronchus fragility during vigorous inspiration. In addition, there was the possibility that the pectus excavatum deformity and severe sternal retraction compressed the right main stem bronchus due to easy collapsibility as mentioned above, also resulting in large negative pressure during inspiration. Such extreme negative pressure in the right lung alveoli could overcome capillary hydrostatic pressure and lymphatic drainage, causing unilateral pulmonary edema. In this case of unilateral pulmonary edema after acute subglottic, it is suggested that subglottic edema
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and coincidental unilateral bronchial obstruction secondary to weakness of bronchial wall caused unilateral pulmonary edema.
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