Ultrasound: Contemporary tool for missed pericardial effusion in a trauma patient

Sir,

Blunt cardiac injuries are often underestimated and missed in view of varied presentation from mild chest discomfort to severe haemodynamic shock. It is potentially difficult to diagnose pericardial effusion in haemodynamically compensated trauma patients. Ultrasound imaging is valuable in the diagnosis of deceptively stable appearance of such trauma patients.

A 58-year-old female with no comorbidity sustained fall from height developing bilateral haemothorax and burst fracture of D9 vertebrae with paraplegia. She was intubated in the emergency room in view of decreasing oxygen saturation. She had bilateral lung contusions (left more than right). Focussed assessment of sonography in trauma (FAST) revealed bilateral moderate pleural effusion. She was shifted to intensive care unit (ICU) with vitals of pulse 90/ min, non-invasive blood pressure of 98/60 mm Hg and central venous pressure (CVP) of 12 cm of water with a normal ECG. On second day of ICU admission, she had two episodes of atrial premature contractions (APC) which resolved on its own. Electrocardiogram (ECG) done showed APCs and poor R wave progression. Serum electrolytes were in normal range and serum albumin was 1.8 mg/dl. CK-MB and CPK were mildly elevated and troponin I was within normal range. Bedside ultrasound (USG) and FAST done for any free fluid incidentally revealed pericardial effusion in the subxiphoid window of FAST [Figure 1] which could have caused APCs and hypotension. Echocardiography confirmed pericardial effusion with no tamponade effect. Diagnosis of blunt cardiac contusion with pericardial effusion was made, which otherwise was missed out on initial admission. Patients were managed conservatively and follow up USG revealed decreasing trend of effusion and no further appearance of any rhythm disorders or hypotension.

Figure 1.

Subxiphoid window of FAST showing pericardial effusion

Blunt cardiac injuries are diagnosed by CK-MB isoenzymes, radioisotope scanning, continuous ECG monitoring, echocardiography and cardiac catheterisation.[1] After the injury, a rise of more than 6% in CPK and CK-MB generally points out cardiac contusion.[2] In patients with significant blunt cardiac injuries, elevated serum troponin I levels correlate with the echocardiographic or electrocardiographic changes. However, these levels have low sensitivity and predictive values in diagnosing myocardial contusion in those without elevation as was in our case.[3] ECG generally shows sinus tachycardia, atrial flutter or atrial fibrillation.[1] Echocardiography may reveal pericardial effusion and decreased myocardial contractility.[1] Special attention must be given to patients receiving mechanical ventilation with positive airway pressure, as this may further decrease cardiac output by reducing the compensatory venous filling pressures.[3] Pericardium can hold up to 150 ml of fluid without increasing intrapericardial pressure.[4] Asymptomatic patients should be observed for 24 hours, but if a patient is in shock or preshock condition and his/her CVP is more than 12 mm Hg, pericardiocentesis should be carried out.[2,5]

Despite simple and effective treatment, the diagnosis of pericardial effusion is often challenging because clinical symptoms can be misleading. Ultrasonography has achieved the role of the contemporary diagnostic tool for the assessment and follow up of traumatic pericardial effusion. Continuous re-evaluation for blunt cardiac injuries in a patient with arrhythmias using USG can prevent further catastrophe.