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Infantile Major Airway Stenosis and Acute Respiratory Distress Associated with Cardiac Tamponade

Mentzelopoulos, Spyros D. MD, PhD, DEAA*†; Tzoufi, Maria MD, DEAA; Kostopanagiotou, Georgia MD, PhD

doi: 10.1213/01.ANE.0000150938.65225.AF
Pediatric Anesthesia: Case Report

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.

IMPLICATIONS: This case indicates that, in young pediatric patients who have undergone corrective or palliative heart surgery, severe and acute pericarditis may result in major airway compromise secondary to external compression and circumferential edema.

*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

Accepted for publication November 3, 2004.

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@hol.gr.

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

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).

Figure 1

Figure 1

Figure 2

Figure 2

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.

Figure 3

Figure 3

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

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.

Figure 4

Figure 4

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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