Background

Pericardial effusion is a known complication of open cardiac surgery with 1–3% of patients needing intervention [1,2,3]. Postoperative pericardial effusion secondary to bleeding into the pericardial sac is commonly identified prior to hospital discharge [1]. Delayed pericardial effusion can arise within a week to 6 months post-cardiac surgery [4, 5]. The progression of this collection as a cause of life-threatening cardiac tamponade can be overlooked because of atypical symptoms and absence of classical echocardiography changes [5,6,7].

Late-onset pericardial effusion is commonly related to post-pericardiotomy syndrome due to inflammation of the pericardium after a cardiac procedure [8]. Loculated effusions are more common in this patient population because of pericardial adhesions or scarring associated with surgery [6, 9]. Inflammation or bleeding may lead to fluid accumulation at the posterior and lateral part of the pericardium, making it difficult to visualize with transthoracic echocardiogram (TTE) [10, 11]. Transthoracic echocardiogram has been identified as a sensitive modality to evaluate the heart for complications after cardiac surgery [12].

In recent years, the usage of TEE has escalated in the emergency department (ED) and critical care, and this trend is well documented in the literature [13,14,15,16,17,18,19,20,21,22]. Focused or resuscitative TEE are terms used to describe the usage of limited TEE views to facilitate early recognition of pathologic processes and to guide clinical decision-making in critically ill patients [13,14,15]. In contrast to the 20-view conventional TEE in a standard cardiology exam, focused TEE utilizes five important views which are the mid-esophageal four-chamber, mid-esophageal long axis, transgastric short axis, bicaval view, and descending thoracic aorta long axis [16, 17]. Focused TEE in the ED is beneficial in the management of cardiac arrest [17, 18] undifferentiated shock [19] and trauma [20, 21]. The use of TEE by non-cardiologists in the ED and intensive care setting for critically ill patients is safe [22] and extremely useful in resource-limited setting [23]. However, focused TEE does not replace the need for comprehensive TEE when clinical questions exceed the scope of a limited exam.

In this case series, we describe the role of resuscitative TEE in managing patients with loculated cardiac tamponade post-coronary artery bypass grafting (CABG) surgery.

Case 1

A 52-year-old male patient presented to the ED with dizziness and breathlessness. He was recently discharged after an on-pump CABG for triple vessel disease. His post-operative recovery was uneventful, and his hospital length of stay was 10 days. On representation to the ED, he was in shock with blood pressure (BP) of 84/45 mmHg, afebrile and pulse rate (PR) of 98 beats per minute with no pulsus paradoxus. He was tachypneic with a respiratory rate (RR) of 24 breaths per minute and oxygen spirometry (SpO2) 97% on room air. On examination, his jugular venous pressure was not elevated. His sternotomy scar was clean and not inflamed. His cardiorespiratory and abdominal examinations were unremarkable. There was no neurological deficit. Echocardiogram showed sinus rhythm without any ischemic changes. Chest X-ray showed cardiomegaly with clear lung fields. His arterial blood gas showed good gas exchange with no metabolic acidosis. The hemoglobin level was 11 g/dL and his coagulation profile was normal. The renal and liver function tests did not show any abnormalities.

The bedside TTE of right ventricle (RV) inflow view showed compression of the right atrium (RA) by a pericardial clot (Fig. 1, Additional file 1: Video S1). Given the TTE findings, TEE was performed by the attending emergency physician and revealed a localized posterior clot measuring 3 × 5 cm compressing the right atrium (Figs. 2, 3, Additional file 2: Video S2, Additional file 3: Video S3 and Additional file 4: Video S4). He was started on intravenous infusion of noradrenaline 0.3 mcg/kg/min for blood pressure support. The patient was diagnosed with possible cardiac tamponade due to loculated posterior pericardial clot and transferred to his previous managing cardiothoracic surgery team which was 200 km away for definitive surgical intervention after cardiology consultation. He made a complete recovery and was discharged after a week.

Fig. 1
figure 1

Transthoracic echocardiogram (TTE) of right ventricle inflow view showed a small and compressed right atrium (yellow arrow). Posterior pericardial clot is not well visualized in this view. IVC inferior vena cava, RA right atrium, RV right ventricle, SVC superior vena cava

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Fig. 2
figure 2

a, b Transesophageal echocardiogram (TEE) at mid-esophageal 4-chamber view with probe rotating to the right showed a compressed right atrium and a posterior pericardial clot measuring about 2 × 5 cm (green watermark). LA left atrium, LV left ventricle, RA right atrium, RV right ventricle

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Fig. 3
figure 3

a, b Transesophageal echocardiogram (TEE) mid-esophageal 4-chamber view showed a compressed right atrium and posterior pericardial clot (green watermark). c, d TEE bicaval view showed similar findings with right atrium compression by an extrinsic posterior pericardial clot (green watermark). LA left atrium, LV left ventricle, RA right atrium, RV right ventricle

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Case 2

A 62-year-old obese diabetic male patient presented to the ED complaining of dizziness and syncope 11 days after an on-pump CABG procedure for left main stem disease. On examination, he was drowsy and tachypneic. He was ill appearing with a BP of 75/42 mmHg, PR 88 beats per minute, without pulsus paradoxus, RR 30 breaths per minute and SpO2 85% on room air. He had a short neck and his neck veins were not prominent. His midline chest wound was well healed. Lung examination showed decreased air entry at the bases. Physical examination of his other systems was unremarkable. Echocardiogram revealed a sinus rhythm without any acute ischemic changes. Cardiomegaly on chest X-ray revealed bilateral basal atelectasis. The patient was intubated for respiratory distress and hemodynamics stabilized with intravenous noradrenaline 0.2 mcg/kg/min. His arterial blood gas showed pH 7.30, PO2 90 mmHg, PCO2 57 mmHg, HCO3 37 mmol/L, and BE 10 mmol/L under a low setting synchronized intermittent mandatory ventilation (SIMV) mode. His complete blood count was normal with hemoglobin of 14 g/dL, white blood count 10 X 109/L and platelet count of 160 × 109/L. Apart from a mildly raised glucose of 14 mmol/L and a baseline raised creatinine of 120 umol/L, his other blood profile values were within a normal range.

Bedside TTE images were suboptimal except for the subcostal view which showed good bi‐ventricular systolic function with trace pericardial effusion (< 1 cm). Other structures could not be evaluated with TTE due to the poor echo window.

Transesophageal echocardiography was performed in ED by attending emergency physician and revealed a large clot localized in the posterior pericardial cavity around the right atrium at the base of the heart (Fig. 4, Additional file 5: Video S5). The clot partially obliterated the right atrium during diastole causing tamponade physiology. The TEE findings were conveyed to an in-house cardiologist. The patient was readmitted to the cardiothoracic surgery for surgical drainage and he made an uneventful recovery.

Fig. 4
figure 4

a, b Transesophageal echocardiogram (TEE) at mid-esophageal 4-chamber view with probe rotating to the right showed a compressed right atrium and a posterior pericardial clot measuring (green watermark). RA right atrium, RV right ventricle

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Discussion

There are several conditions that can cause hemodynamic instability in post-cardiac surgery patients, with their own unique treatment pathways. These conditions include failed graft, sepsis, bleeding, pulmonary embolism, tamponade and cardiac arrhythmias. Therefore, rapid stabilization and diagnosis are crucial for life-saving interventions to be performed. However, assessment of these undifferentiated post-cardiac surgery patients is challenging due to non-specific symptoms and signs as in the cases described earlier.

In the pathophysiology of cardiac tamponade of any cause, increased intrapericardial pressure exceeds the intracardiac pressure causing compression of the adjacent cardiac chamber [24]. Pericardial effusion after cardiac surgery may be loculated due to a pericardial adhesion that may lead to selective chamber compression [5]. Constant high left ventricular pressure in the isolated right-sided chamber compression may explain the absence of classical signs of cardiac tamponade such as pulsus paradoxus, transmitral and transtricuspid flow variability [25].

Low-pressure cardiac tamponade physiology can also occur in post-cardiac surgery patients. This is due to medication-induced reduction in filling pressures by the use of diuresis and vasodilators [24]. The suppression of the compensatory sympathetic stimulation by beta-blockers may also contribute to the atypical presentation of these patients.

Both our patients presented more than a week after CABG. Apart from the obvious signs of shock, clinical examination, conventional bedside tests such as electrocardiogram and chest X-ray did not give much clue to the cause of hypotension. Point-of-care ultrasound was used to assess the volume status, determine heart function and exclude the life-threatening diagnosis.

In the first case, the TTE image was inconclusive and showed a small right atrium with posterior hyperechoic structure suggestive of compression from the extracardiac source. With this finding, a high index of suspicion that a localized pericardial effusion was present prompted the decision to proceed with TEE. In the second case, the patient was immediately intubated and stabilized with inotropic support upon arrival at the ED.

Cardiac tamponade is a complication of post-cardiac surgery that may be difficult to assess using TTE [11, 12]. Identifying loculated pericardial effusions and clotted blood in the pericardium can be challenging [12]. Typical ultrasound features found in usual cardiac tamponade cases such as right atrial systolic collapse, right ventricular diastolic collapse, swinging heart and plethoric inferior vena cava may be absent. Transesophageal echocardiography is not limited by chest wall-related barriers and may provide life-saving diagnostic information in this patient cohort.

Conclusion

Cardiac tamponade secondary to loculated posterior pericardial clot is a life-threatening cause of hemodynamic instability in the post-CABG patient. Transesophageal echocardiography may be of limited utility because of patient-level post-surgical variables. Transesophageal echocardiography performed in the ED can allow for a rapid diagnosis, an early referral and an opportunity to institute appropriate therapeutic measures in this challenging patient population.