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.
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.
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.
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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