A 10-month-old boy presents to the ED with a 1-day history of poor feeding and a fluctuating level of consciousness. There has been no fever, vomiting, diarrhea, or cough.
On physical examination, the child looks ill and mottled. His temperature is 101.5°F (38.6°C), heart rate is 180 beats/min, respiratory rate is 60 breaths/min, blood pressure is 70/40 mm Hg, and oxygen saturation is 86% in room air. He requires 10 L of oxygen to maintain his oxygen saturation above 95%. His heart sounds are normal, capillary refill is 3 seconds, and femoral pulses are weak. Both lungs are clear, and the liver is palpable 5 cm below the right costal margin. The remainder of the physical findings are normal.
The patient is given a 20-mL/kg bolus of normal saline intravenously as well as ceftriaxone. The hypotension does not improve. Initial laboratory findings are: WBC count, 66.4x103/mcL (66.4x109/L) (polymorphs 64%, bands 15%, lymphocytes 10%); Hgb, 1.06 g/dL (106 g/L); and platelets, 848x103/mcL (848x109/L). The bedside glucose value is normal. Venous gas measurements include: pH, 7.23; PCO2, 42 mm Hg; bicarbonate, 17 mEq/L (17 mmol/L); and base excess, –9 mmol/L. Serum lactate is 72.1 mg/dL (8.0 mmol/L). A chest radiograph reveals a small left-sided infiltrate, a small pleural effusion, and a normal heart size. ECG shows small voltages, ST segment elevation in leads V2 through V5, and electrical alternans. A diagnostic test is performed.
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Cardiac involvement was suspected on initial assessment when the liver was noted to be enlarged. Furthermore, the child did not respond clinically to the fluid bolus, as would be expected in hypovolemic shock or septic shock without cardiac involvement. The electrocardiographic findings were highly suspicious for cardiac tamponade, and a bedside echocardiogram revealed a large pericardial effusion measuring 3 cm in diameter. Pericardiocentesis yielded 60 mL of purulent pericardial fluid, after which the patient’s blood pressure and perfusion improved almost instantaneously. Subsequent blood and pleural fluid cultures grew Streptococcus pneumoniae.
Differential Diagnosis
This child presented with a fluctuating level of consciousness and was found to be in shock on initial assessment. The differential diagnosis of his clinical picture is broad and includes septic shock, hypovolemic shock, hemorrhagic shock, cardiogenic shock, neurogenic shock, toxic ingestion, and nonaccidental injury. Echocardiography demonstrated the cause of this child’s shock to be cardiac tamponade from a large pericardial effusion.
Acute pericarditis with pericardial effusion in children can be caused by bacterial infection, viral infection, collagen vascular disease (systemic lupus erythematosus), malignancy, metabolic disease, or postpericardiotomy syndrome. In some cases, no cause can be found. Bacterial (purulent) pericarditis in childhood is caused most commonly by Staphylococcus aureus. The next most common pathogens are Neisseria meningitidis, Haemophilus influenzae, and S pneumoniae.
Pathogenesis
Patients who develop bacterial pericarditis are found frequently to have preceding or concurrent infections, including pneumonia, osteomyelitis, meningitis, septic arthritis, pyomyositis, and pyelonephritis. This child had radiographic evidence of pneumonia with a small pleural effusion. Bacteria are believed to invade the pericardium by direct extension from the neighboring pleura or lung or from transmission through the blood from another infected site. In some cases of meningococcal meningitis, an immunologically induced antibody response to the bacterial infection causes inflammation and fluid accumulation within the pericardial space. The discovery of pericarditis several days after the onset of infection and the absence of bacteria in the pleural fluid supports this mechanism.
Clinical Presentation and Diagnosis
Pericardial effusion with tamponade is diagnosed clinically by signs such as tachycardia, hypotension, elevated jugular venous pressure, muffled heart sounds, hepatomegaly, narrow pulse pressure, and pulsus paradoxus (systolic blood pressure during inspiration is lowered markedly). A pericardial friction rub may be present as well, but is less common in larger effusions where the large amount of fluid prevents friction. The presence of an enlarged cardiac shadow on chest radiography is supportive, as are the ECG findings of low voltages, raised ST segments, and when cardiac tamponade is present, electrical alternans. Electrical alternans, defined by the QRS amplitude increasing and decreasing on alternate beats, is caused by the beat-to-beat swinging motion of the heart with large pericardial effusions (Figure). Definitive diagnosis is made by echocardiography, which is safe, rapid, and noninvasive and has a high degree of sensitivity for the detection of pericardial effusion. The hallmark of the echocardiographic diagnosis of pericardial tamponade is diastolic collapse of the atrial and ventricular walls.
Treatment
Bacterial pericarditis is treated with specific antibiotics, which should be selected to target the suspected organism. Associated infection or illness can provide guidance in the selection. Pericardiocentesis is indicated to relieve the symptoms of cardiac tamponade. Rapidly accumulating effusions are more likely to present with symptoms. Pericardiocentesis also is useful for diagnostic purposes; pleural fluid can be sent for cytologic and biochemical analysis as well as culture for bacteria, fungi, and viruses. Except in emergencies, this procedure should be performed by a cardiologist, cardiovascular surgeon, or thoracic surgeon under echocardiographic guidance. Diuretics are contraindicated in the setting of symptomatic cardiac tamponade because the cardiac output is highly dependent on ventricular filling. By the same token, endotracheal intubation and mechanical ventilation can cause an acute decrease in ventricular filling that may lead to sudden cardiac arrest.
Conscious sedation and analgesia are recommended when performing pericardiocentesis. Under aseptic conditions, an 18-gauge needle is attached to a three-way stopcock and a 50-mL syringe. The needle is inserted just under the xiphoid process, directed toward the left shoulder tip, and advanced with constant suction. The heart should be monitored during the procedure, enabling the detection of arrhythmias that may occur when the myocardium is touched. Other techniques have been described in the literature, including subxiphoidal tube drainage and irrigation with thrombolytics, as well as pericardiectomy. Pericardiectomy usually is reserved for patients who have loculated effusions or recurrent pericarditis and are at higher risk for constrictive pericarditis.
Lessons for the Clinician
When a patient presents with clinical signs of shock, the clinician should examine the patient carefully for signs of cardiac tamponade. If clinical signs are present, immediate chest radiography should be performed to determine heart size and an ECG obtained to assess for small voltages, ST segment changes, and electrical alternans. Echocardiography is essential for definitive diagnosis and for facilitating guided pericardiocentesis to relieve cardiac tamponade.
Adam Cheng, MD
Jennifer Russell, MD
The Hospital for Sick Children, Toronto, Ontario, Canada