Pericardial effusion has multiple causations with varying content and clinical presentations. An unusual cause for pericardial effusion is illustrated here. The patient was an elderly female, who presented with epigastric abdominal pain and subsequently developed hypotension. Bedside ultrasound performed as per the RUSH (rapid ultrasound for shock and hypotension) protocol showed significant pericardial fluid with good cardiac contractility but no tamponade physiology yet. A CT Aortogram was done for suspicion of aortic dissection in view of significant pericardial effusion and mainly upper abdominal pain which showed a foreign body lodged within the distal oesophagus, causing an oesophageal perforation with associated moderate amount of pericardial effusion.

The pericardial space is contained between the visceral and parietal layers of the pericardium and normally contains 20-60 mL1 of serous fluid normally. Any accumulation of additional fluid causes a condition of pericardial effusion. Once the total volume within the pericardial space reaches the point at which the intrapericardial pressure is significantly high and either compromises the venous return or the cardiac output or both, it results in a cardiac tamponade. Generally, gradually accumulating large volumes of pericardial effusions are well tolerated than rapidly accumulating pericardial effusions of even 150-200 mL and can cause life-threatening condition of cardiac tamponade. The case highlights one of the unusual causes of pericardial effusion and a high index of suspicion is required for its diagnosis in the emergency department.

Our patient was an elderly lady in her mid-90s who had a medical history of diabetes mellitus, hypertension, hyperlipidaemia, mild to moderate cognitive impairment and anaemia. She was on regular dose of 100 mg Aspirin every morning for a diagnosis of presumed Ischemic Heart Disease (IHD). She presented with a vague sounding epigastric abdominal discomfort and a “bloated” sensation of few hours and complained of “feeling weak” and “almost blacked out” while going to the toilet. She appeared very pale to the family members while attempting to sit on the toilet bowl and had faecal and urinary incontinence as well then. She denied any vomiting, diarrhoea, dysuria, chest pain or difficulty in breathing then.

On clinical examination, she was afebrile, her respiratory rate was 18 breaths/minute, her pulse rate was 108 beats/minute, her blood pressure was 102/58 mm Hg, pulse oximetry SpO2 on room air was 99%. The verbal numerical pain scale was 2/10. She was alert, conscious, conversant and speaking in full sentences then. She appeared to be in some discomfort then. Systems examination wise, her heart sounds were dual and there were no murmurs audible then. The lung sounds were clear. Her abdominal exam was remarkable for mild right hypochondriac and epigastric tenderness. There were no masses felt and the bowel sounds were audible. The renal punch was negative bilaterally. On digital rectal examination, there was no blood seen, no melaena, no masses were felt and the anal tone was intact. She was moving all her limbs with normal motor power and the sensation was symmetrical and normal. An ECG (Figure 1) was performed upon her arrival which was similar to her baseline ECG. There were no new gross ST segment elevations or depressions

Figure 1: 1st ECG after arrival

After her initial consult and while awaiting blood investigation reports, she complained of giddiness and near fainting and was noted to be hypotensive with systolic BP in 80s. Fluid bolus was started immediately. Bedside ultrasound performed as per the RUSH protocol showed moderate amounts of pericardial effusion measuring about 2.4 cm in maximum width. Minimal indentation of the Right Ventricle wall was noted during diastole which was not consistently observed. The cardiac contractility was good and the right ventricle was not dilated. There was no intraabdominal free fluid and abdominal aorta was less than 3 cm in the entire length. The IVC (inferior vena cava) had nil variability on respiration and appeared plethoric. An ECG was repeated as well which was largely unchanged from the previous one.

The systolic blood pressure improved to 110 mm Hg after a fluid bolus of 500 mL. A Chest X-ray done showed an enlarged heart shadow in the antero-posterior projection with minimal bilateral pleural effusions.

A CT Aortogram (Figure 2 & Figure 3) was then done to rule out an aortic dissection at this point of time. The CT Aortogram showed a 3 cm foreign body lodged within the distal oesophagus, with its anterior tip abutting the base of the heart. Features were highly suspicious for oesophageal perforation complicated by moderate hemopericardium, mediastinal haematoma and small bilateral hemothoraces (larger on the right). There was no pneumomediastinum. There was no evidence of significant aortic aneurysm, aortic dissection or penetrating ulcer seen.

Figure 2: Significant Pericardial Effusion seen in the CT Aortogram in the Axial view

Further history from the family members suggested that the patient had eaten fish recently and was also noted to have an episode of mild hematemesis after that.

Laboratory Investigations (Table 1) were as follows:

Figure 3: Foreign Body (indicated by the red arrow) seen lodged in the distal Oesophagus and abutting the heart

Further history from the family members suggested that the patient had eaten fish recently and was also noted to have an episode of mild hematemesis after that.

Laboratory Investigations (Table 1) were as follows:

Table 1: Relevant Laboratory Investigations

Patient was admitted under the Cardiology ward in a monitored bed as there was a diagnosis of possible concomitant Non ST Elevation Myocardial Infarction (NSTEMI) as well. Surgical team was consulted immediately and plans discussed were of removal of the fish bone by endoscopic procedure likely followed by a definitive surgery via thoracotomy, chest drain insertion, primary repair with possible esophagectomy if needed and pericardium repair. The risk of mortality and possible complications from endoscopy was moderate and risk of mortality and possible complications from a surgical procedure was high. Patient was started on relevant medical management via intravenous broad spectrum anti-biotics and proton pump inhibitors and kept nil by mouth in anticipation of any procedure/intervention. Family was hesitant for any therapeutic intervention and eventually decided not for any invasive intervention and instead chose to seek some form of comfort care for the patient. Geriatric and Palliative care speciality services were involved thereafter and patient was allowed diet as tolerated. She was started on subcutaneous Fentanyl infusion as well bolus Fentanyl as required for breakthrough pain and dyspnoea episodes. A do-not- resuscitate (DNR) plan was established for the patient as per the family’s wishes. Patient expressed wishes to perform her prayers at home and she was allowed a home leave. Subsequently, she passed away peacefully at her home on day 6 of her illness.

Cases of foreign body oesophageal perforations [2] leading to pericardial effusion, and even tamponade have been reported in the literature previously. Virtually any disease that can involve the pericardium, can cause a pericardial effusion. Hence, there are multiple causes of a pericardial effusion. Pericardial effusions that are most likely to cause cardiac tamponade include those due to infectious causes, haemorrhage and malignancies. Gradually accumulating pericardial effusions can mostly be asymptomatic unless they are very large in volumes or have accumulated rapidly causing a cardiac tamponade which causes dyspnoea, tachypnoea, tachycardia and symptoms and signs of hypoperfusion along with muffled heart sounds, pulsus paradoxus, and an elevated jugular venous pressure. Patients may also experience right upper quadrant abdominal discomfort due to hepatic congestion. Patients may also have symptoms and signs of one of the many underlying diseases that caused the pericardial effusion. In the absence of tamponade, the cardiovascular examination is normal except in cases of large effusions when it may be difficult to palpate the cardiac impulse and the heart sounds may be muffled.

On ECG, the main abnormalities are reduced voltage and electrical alternans [3] both of which occur with large effusions.

Some selected causes [4,5] of pericardial effusion are infections, inflammatory causes, vasculitis, drug induced, post myocardial infarction, hemopericardium & trauma, dissecting aortic aneurysm, iatrogenic [6,7] malignancy, radiation therapy, chronic renal failure, chylopericardium, stress-induced cardiomyopathy, hyperthyroidism or hypothyroidism and idiopathic [8].

In an emergency department, bedside ultrasound is the imaging modality of choice for evaluation of pericardial effusion as well as a tamponade physiology. It can give additional information about abdominal aortic aneurysms and intraabdominal free fluid as well inferior vena cava fluid responsiveness status. The differentiation between small, medium and large pericardial effusions is based on the echocardiographic appearance and the estimated volume of the effusion. Small effusions usually have 50-100 mL (end-diastole<10>500 mL (or >20 mm on echo). Ultrasound is also used to plan and guide periocardiocentesis [9]procedure in the emergency department, as it can help in locating the best  site  for  drainage  and  insertion  of  the  pericardiocentesis needle.

Although the success is largely operator dependent, the subxiphoid approach is most commonly used. An apical site approach may also be used and in some cases is the preferred site for drainage. Open surgical pericardiocentesis is rarely the initial method for removal of fluid. It is mainly reserved for bleeding due to trauma or rupture of the left ventricular free wall, loculated effusions, and recurrent effusions severe enough to cause tamponade that require establishment of a pericardial window for therapeutic purposes and tissue sampling for diagnosis. In the absence of pericardial tamponade and high risk pericardial effusions like those from trauma or ventricular free wall rupture in STEMI, in most of the cases of pericardial effusion drainage is of little therapeutic benefit. Medical treatment [10] of nonthreatening effusions should be based on the suspected underlying cause. Many of these effusions resolve spontaneously. The prognosis [11] is mostly dependent upon the size of the effusion and the causation. Infectious causes like bacterial and fungal effusion, neoplastic effusions, traumatic and post dissection effusions and post myocardial effusions in general have guarded prognosis and may be associated with higher mortality and morbidity. Pericardial effusions secondary to acute idiopathic pericarditis, especially when small, have an excellent prognosis.

Acute pericardial effusion is a potentially life threatening situation if it accumulates rapidly and leads to a cardiac tamponade. In this case, the amount of hemo-pericardium was moderate to large, resulting from a foreign body lodged in the oesophagus causing a perforation and peri- myocardial injury. Unfortunately, this patient mainly due to being very elderly in 90s, was deemed a very high risk surgical candidate, since either needle pericardiocentesis or endoscopic removal of the foreign body alone was not a curative option in her case. This case brings into focus an unusual and rare cause of pericardial effusion and how a diligent assessment and optimal use of bedside ultrasound can provide very useful clinical information and diagnosis many a times. Also a high index of suspicion is required to choose appropriate investigations early to diagnose the causation of the pericardial effusion in patients who present with uncommon clinical symptoms.