Anesth Analg 2005;100:1627-1630
© 2005 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000150938.65225.AF
PEDIATRIC ANESTHESIA
Infantile Major Airway Stenosis and Acute Respiratory Distress Associated with Cardiac Tamponade
Spyros D. Mentzelopoulos, MD, PhD, DEAA*
,
Maria Tzoufi, MD, DEAA, and
Georgia Kostopanagiotou, MD, PhD
*Department of Pediatric Cardiac Anesthesiology, Agia Sofia Children’s Hospital; and Department of Intensive Care Medicine and Second Department of Anesthesiology, University of Athens Medical School, Attikon University Hospital, Athens, Greece
Address correspondence and reprint requests to Spyros D. Mentzelopoulos, MD, PhD, DEAA, Department of Intensive Care Medicine, Attikon University Hospital and Department of Pediatric Cardiac Anesthesiology, Agia Sofia Children’s Hospital, 12 Ioustinianou St., GR-11473, Athens, Greece. Address e-mail to sdm{at}hol.gr.
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Abstract
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Coxsackie virus pericarditis caused cardiac tamponade in a 45-day-old infant with corrected total anomalous pulmonary venous drainage and a hypodynamic left heart. The pathophysiology comprised reduced heart compliance, venous return impairment, acute pulmonary hypertension, and increased airway microvascular permeability. Tracheal edema and external compression caused tracheal lumen narrowing and respiratory failure. Laryngoscopy was difficult because of laryngeal inlet swelling. Endotracheal intubation was accomplished with a 3.0-mm tube. Pericardial cavity evacuation resulted in rapid recovery. A postprocedural chest radiograph revealed tracheal lumen enlargement. Repeated laryngoscopy revealed resolution of upper-airway edema. In infants, large pericardial effusions developing after corrective/palliative heart surgery may cause major airway compromise.
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Introduction
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Obstruction of the left mainstem bronchus secondary to purulent pericarditis has been reported (1). We report a case of viral pericarditis/probable postpericardiotomy syndrome (2) and severe tracheal stenosis and laryngeal inlet swelling in an infant with recent surgical correction of a congenital cardiac defect. Airway pathology was reversed immediately after pericardial cavity evacuation.
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Case Report
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A 45-day-old, 4.1-kg, male infant was admitted to the hospital because of sudden onset respiratory distress. Rapidly worsening cyanosis had ensued within 24 h of admission. Seven days before admission, the patient had developed symptoms of an upper respiratory tract infection (coryza, cough, and fever up to 38.5°C), which lasted 4 days. The patient’s history was significant for a surgical correction of type II (cardiac) total anomalous pulmonary venous drainage with restrictive atrial septal defect on the 27th day of life, and the patient was discharged 10 days after the operation. Just before the hospital discharge, the patient’s systolic pulmonary artery pressure (continuous-wave Doppler) had been estimated at 67 mm Hg, and the peripheral oxygen saturation (Spo2) was 
90% in room air. On clinical examination at the time of readmission, the patient was cyanotic and tachypneic. Chest auscultation revealed bilaterally diminished breath sounds and muffled heart tones. His Spo2 was 60%–65% while breathing 50% oxygen and increased to 80%–82% on 100% oxygen, and his arterial blood pressure was 51/26 mm Hg, heart rate was 175–185 bpm, and the axillary temperature was 37.9°C. An emergency chest radiograph on admission revealed a cardiac shadow enlargement and a mediastinal widening; the radiolucent line, corresponding to the extra- and intrathoracic trachea, was almost absent (indicating severe tracheal lumen stenosis) (Fig. 1). Transthoracic echocardiography revealed a large pericardial effusion (Fig. 2A), measuring 20–25 mm, in its coronal diameter, and the right and left ventricular diastolic diameters increased and decreased during inspiration, respectively. During diastole, the right ventricle was distended, the interventricular septum was shifted to the left, and the free left atrial wall exhibited inward movement (Fig. 2B). Right ventricular distention, despite the severe pericarditis, was caused by concomitant pulmonary hypertension. Systolic pulmonary artery pressure (continuous-wave Doppler) was estimated at 111 mm Hg (Fig. 2C). Visualized major pulmonary vessels were engorged (Fig. 2D).
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Figure 1. Emergency chest radiograph on cardiothoracic intensive care unit admission. The cardiac shadow is enlarged, and the mediastinum is widened. The lumen of the trachea (white arrows) appears severely stenosed. The long black arrow indicates the direction of the plane of the ultrasonographic section presented in Figure 2D. The transducer was placed in the second right intercostal space, approximately 1.5 cm laterally to the edge of the sternum and directly above a small area of apical atelectasis (AA). The axis of the ultrasonographic sector arch was directed inferiorly and posteromedially. The atelectasis was probably caused by segmental/subsegmental bronchus compression by the engorged pulmonary arterial vessels (see also main text and Fig. 2D).
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Figure 2. Emergency transthoracic echocardiography at cardiothoracic intensive care unit admission. (A) Subcostal view revealing a large amount of pericardial fluid compressing the right and left ventricles. (B) Four-chamber view during diastole. The right ventricle and atrium are dilated, and the interventricular septum is shifted to the left. Note the inward movement of the free wall of the left atrium (arrow); this finding is highly specific for cardiac tamponade (3). (C) Continuous wave Doppler estimation of systolic pulmonary artery pressure (= 4 x [5.28]2 = 111.4 mm Hg) by determination of peak systolic blood flow velocity (5.28 m/s) along the axis (A) of the tricuspid valve. (D) High intercostal and oblique view of the right pulmonary artery and its superior branch; the solid-appearing area of echogenicity surrounding the imaged pulmonary arterial vessels corresponds to atelectatic lung parenchyma (Fig. 1); the end-systolic transverse diameter of the right pulmonary artery (highlighted by the thin white line) amounts to  9 mm. LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle; S = interventricular septum; PF = pericardial fluid; TRV = tricuspid valve; A = axis of flow velocity measurement; RPA = right pulmonary artery; SRPAB = superior RPA branch; P = pericardium; AAO = ascending aorta.
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Cardiac tamponade and critical major airway stenosis were diagnosed. The patient was brought to the operating room for emergency pericardiocentesis under general endotracheal anesthesia. Inotropic support with dobutamine (5–10 µg · kg–1 · min–1) was started, and anesthesia was then induced with ketamine (2 mg/kg). On direct laryngoscopy, the epiglottis and arytenoids were swollen, and the vocal cords were not visible. A 3.0-mm internal diameter (ID) endotracheal tube (ETT) was passed into the larynx and trachea only after external laryngeal manipulation could allow for posterior glottis exposure. Immediately after tracheal intubation, there was no spontaneous respiration, and the patient’s lungs were mechanically ventilated (Siemens Servo Ventilator 900C, Berlin, Germany; mode, pressure-controlled; inspired oxygen fraction, 80%; pressure control level, 20 cm H2O; respiratory rate, 35–40 breaths/min; positive end-expiratory pressure, 0 cm H2O) with no audible inspiratory gas leak at peak pressures of 20 cm H2O. The Spo2 increased to 100% within 3 min. Spontaneous respiration was then restored, and the patient was allowed to breathe 60% O2 in air via a T-piece.
A paraxiphoid pericardiocentesis resulted in drainage of 65 mL of serous pericardial fluid. A pigtail catheter was placed into the pericardial cavity for continuous drainage. The procedure was performed with the patient breathing spontaneously and maintaining an Spo2 of >95%. Analgesia was maintained with 2 0.5-mg/kg ketamine boluses. The postprocedural chest radiograph revealed diminution of the cardiac shadow and an enlargement of the tracheal diameter (to 4–5 mm) (Fig. 3A). Arterial blood gas analysis revealed Pao2, Paco2, pHa, HCO3, and lactate of 109 mm Hg, 46 mm Hg, 7.38, 25 mEq/L, and 5 mmol/L, respectively.
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Figure 3. Imaging studies after the evacuation of the pericardial cavity. (A) Chest radiograph performed 15 min after the pericardiocentesis. Note the reduction in the size of the cardiac shadow and the increase in the width of the tracheal lumen (highlighted by the thin white arrows) relative to Figure 1. The thin black arrows point toward the sides of the original, 3.0-mm internal diameter (ID) endotracheal tube (ETT), whereas the thick white arrow points toward the tip of a pigtail catheter left within the pericardial cavity for continuous drainage. (B) Transthoracic echocardiography 2 h postextubation. Continuous wave Doppler estimation of systolic pulmonary artery pressure (= 4 x [3.30]2 = 43.5 mm Hg) by determination of peak systolic blood flow velocity (3.30 m/s) along the axis (A) of the tricuspid valve. The pulmonary artery pressure is still supranormal, despite the reversal of the acute pathophysiology (see also text). RA = right atrium; RV = right ventricle; TRV = tricuspid valve; A = axis of flow velocity measurement.
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After completion of the pericardiocentesis, ketamine (2 mg/kg) was readministered, and direct laryngoscopy was performed to confirm resolution of upper airway edema. On reinstitution of mechanical ventilation, a clearly audible leak ensued at peak airway pressures of >10 cm H2O, and the expired tidal volume was 50%–60% of inspired tidal volume. During the repeat laryngoscopy (performed 30 min after the pericardiocentesis), the anterior commissure of glottis was visible, and the epiglottis and arytenoids were no longer swollen. The original ETT was replaced by a 4.0-mm-ID ETT. Fifteen minutes after ETT change, the patient’s trachea was extubated. Two hours postextubation, systolic pulmonary artery pressure was estimated at 44 mm Hg (Fig. 3B).
Antiinflammatory treatment with indomethacin was initiated, and the pigtail catheter was removed after 72 h. Serology was positive for immunoglobulin M antibodies against Coxsackie B virus. Twenty-four hours later, the patient was transferred to the department of internal medicine, from which he was discharged after another 6 days.
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Discussion
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Cardiac tamponade is characterized by increased pericardial pressure, compression of cardiac chambers, and hemodynamic instability or collapse (3,4). Venous return is mainly systolic (4), and venous pooling occurs (3). In the present case, observed cardiorespiratory and upper airway abnormalities resulted from the underlying pathophysiology (Fig. 4). The preexisting pathophysiology included a hypertrophic/hyperdynamic and noncompliant right heart, with supranormal pulmonary artery pressure, and a hypodynamic and noncompliant left ventricle (5–7) (Fig. 3B). The acute pathophysiology of a large pericardial effusion resulted in pericardial constraint (3,4). Constraint effects on hypodynamic left heart performance were probably exaggerated, with consequent blood pooling in the pulmonary circulation. Tracheal and lung compression by the enlarged pericardial cavity (8) resulted in increased work of breathing, hypoxemia and hypercarbia, increased pulmonary vascular resistance and pressure, and engorgement of main pulmonary arteries (Fig. 2D), with probable further tracheal compression (8). Acute pulmonary artery pressure increase (Figs. 2B and 3B) and pericardial constraint resulted in a dilated and noncompliant right heart, with associated decreases in systemic venous return. Venous pooling and increased airway microvascular permeability secondary to Coxsackie virus-induced inflammation (9,10) could have contributed to laryngeal inlet swelling and circumferential airway edema.
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Figure 4. Schematic presentation of the interaction between preexisting and acutely ensuing pathophysiology. Arrows reflect the speculated temporal sequence of the pathophysiological mechanisms: earliest, first to latest, last. Note that later-occurring pathophysiology further induces earlier-occurring and preexisting pathophysiology, thus resulting in a vicious cycle(s).
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Pericardial cavity evacuation, with improvement in systemic venous return and reversal of preprocedural hypoxemia and hypercarbia, resulted in rapid and simultaneous alleviation/reversal of upper airway pathology and acute pulmonary hypertension. In addition, normalization of the pericardial cavity size and reversal of the major pulmonary vessel engorgement seemed to have resulted in relief of external tracheal compression (8).
In conclusion, in infants subjected to corrective or palliative heart surgery, the acute development of large pericardial effusions may cause tracheal stenosis, laryngeal inlet swelling, and difficulties with airway management.
The authors thank cardiologist L. Ralidis, MD, for offering useful comments on the revised manuscript.
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Footnotes
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Accepted for publication November 3, 2004.
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References
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- Lake CL. Anomalies of the systemic and pulmonary venous returns. In: Lake CL, ed. Pediatric cardiac anesthesia. 3rd ed. Stamford, CT: Appleton and Lange, 1998:373–406.
- Jaumin P, Rubay J, Moulin D, et al. Total anomalous pulmonary venous connection. Long-term results following repair under 3 months of age. J Cardiovasc Surg (Torino) 1989;30:11–5.[Medline]
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Abstract
Introduction
