**3.2 Acute pericarditis**

*Inflammatory Heart Diseases*

two layers: an inner visceral layer which is thin, adherent to and continuous with the epicardium of the heart and an outer parietal layer which is thicker and more fibrous. Normal pericardial thickness is 1–2 mm [8]. The parietal and visceral layers are separated by a small amount of serous fluid [1–8]. In non-disease states, approximately 15–50 ml of fluid is contained within the pericardial sac. This fluid is produced by visceral mesothelium cells and is drained from the pericardial space

The pericardium is fixed in its anatomical position to the diaphragm and sternum via the pericardio-phrenic and sterno-pericardial ligaments, respectively [4]. Posteriorly, the loosely bound connective tissue anchors it to structures contained

Vascular supply is from the pericardio-phrenic artery which is a branch of the internal thoracic artery. Venous drainage is via the pericardio-phrenic veins which drain into the brachiocephalic veins bilaterally. The phrenic nerve provides sensory

The reflections of the pericardium surrounding the great vessels form two potential spaces called the oblique and transverse sinuses which can be visualised on echocardiographic imaging [4, 8]. The larger oblique sinus forms posteriorly between the left atrium and pulmonary veins. The transverse sinus too lies behind the left atrium, posterior to the aorta and pulmonary trunk [4]. Both sinuses are common sites for blood to collect post-cardiac surgery. Because of the formation of these two sinuses, the left atrium is not entirely an intra-pericardial structure.

Although normal cardiovascular function can occur in the absence of the pericardium, it does bestow certain physiological benefits [1–8]. Because of its relatively fixed ligamentous attachments, the pericardium stabilises the heart in its anatomic position and limits excessive movement within the chest cavity particularly with changes in body position. The pericardial fluid minimises friction exerted on the epicardium from normal heart movements during the cardiac cycle and serves to balance hydrostatic pressures over the surface of the heart. The pressure exerted on the cardiac chambers by the pressure within the intra-pericardial space prevents acute distention of the chambers and helps optimise atrial and ventricular coupling and filling. The pericardial sac serves as a physical barrier against the spread of infection or neoplastic disease within the mediastinum. Prostaglandins secreted by mesothelial and endothelial cells of the pericardium regulate autonomic cardiac reflexes, modulate myocardial contractile function and influence epicardial coro-

There are a number of pericardial pathologies which can be a cause for concern

Congenital defects are rare, usually associated with other cardiac, pulmonary and skeletal abnormalities, and are often only found at autopsy with an incidence of 1:10,000 [9]. The absence of the pericardium is more commonly partial with the left side being affected about 70% of the time. Left-sided defects predispose to herniation of the heart which may become haemodynamically significant during

innervation and the sympathetic trunks' vasomotor innervation [4].

**2.2 Normal physiology and functions of the pericardium**

via the lymphatic system to the right side of the heart.

within the posterior mediastinum.

**68**

nary artery tone.

**3. Pathology**

**3.1 Congenital defects**

in the peri-operative period [2–4, 9, 10].

Acute pericarditis is an inflammatory disease of the pericardium lasting less than 6 weeks and the most common pericardial pathology encountered in clinical practice [6, 9–16]. It may be a self-limiting benign condition or the first presentation of an underlying infectious or neoplastic disease process. In this setting, it is prudent to postpone elective surgery for diagnosis and initiation of appropriate treatment.

Causes of acute pericarditis vary widely and may be idiopathic, infectious, non-infectious or autoimmune. The most common causes encountered in the perioperative period are non-infectious post-cardiac surgery, associated with trauma, uraemia in patients with chronic renal failure or post-myocardial infarction.

Symptoms include a sharp left precordial or retrosternal chest pain which may be pleuritic in nature and varies with posture, being decreased on sitting and increased on lying supine. The pain may radiate to the trapezius ridge. This pain referral is due to the involvement of the phrenic nerve which traverses the pericardium and supplies its sensory innervation. Often there are associated prodromal symptoms of malaise, fever and generalised myalgia. Tachycardia and tachypnoea are usually out of proportion to the low grade fever. A tri-phasic friction rub corresponding to atrial systole, ventricular systole and rapid early filling during diastole may be present on examination.

In the peri-operative period, differentiating between acute pericarditis and other causes of chest pain is of utmost importance. Careful clinical examination and special investigations should be carried out to make the correct diagnosis and allow for the institution of appropriate treatment. Three of the more important differential diagnoses are acute coronary syndrome, aortic dissection and pulmonary embolism.

Patients suffering from pericarditis associated with bacterial or fungal infections, malignancies, end-stage renal disease or post-cardiac surgery are at an increased risk to progress to pericardial effusion and tamponade [12].

*Post-cardiac injury syndromes*, also known as post-pericardiotomy syndromes, are being recognised as an important cause for pericardial disease [13, 14]. This clinical syndrome is characterised by a febrile illness associated with pleuritic chest pain and effusions of the pleura and pericardium. The initiating event is an injury to the pericardium, myocardium and pleura from ischaemia, post surgery or a noniatrogenic traumatic event. In predisposed individuals, an autoimmune-mediated response is triggered that can vary from a simple, self-limiting pericarditis to a complicated pleuropericarditis, resulting in massive pericardial and pleural effusions with tamponade.

Special investigations would include a 12-lead electrocardiogram (ECG) which will show sinus tachycardia, PR interval depression and diffuse concave upward sloping ST-segment elevation. Transthoracic echocardiography (TTE) may show an associated pericardial effusion and tamponade as well as other cardiac or paracardiac diseases.

Treatment for acute pericarditis remains symptomatic with non-steroidal anti-inflammatory drugs (NSAIDs) for pain and potentially adding colchicine as an adjunct to prevent recurrence [15]. Low-dose corticosteroids may also be introduced by the primary care team if there is an associated autoimmune disease or in the case of a post-cardiac injury syndrome [13, 14, 16].

### **3.3 Chronic pericarditis**

Chronic pericarditis may be a result of the progression of acute disease or due to recurrent episodes of relapse [6, 9, 10]. The peri-operative management will depend on haemodynamic consequences the disease process has on patient physiological parameters.

Differentiation should be made between chronic pericarditis with ongoing inflammation, pain and fever, relapsing disease where patients have periods of being symptom free and chronic pericardial effusion with persistent fluid accumulation within the pericardial sac.

As with acute pericarditis, all elective surgery should be postponed to enable symptomatic treatment of attacks with NSAIDs, colchicine and corticosteroids. Pericardiectomy is indicated in patients with frequent and severe symptoms that are unresponsive to maximal medical therapy [6, 9].

Chronic inflammatory disease may be associated with a pericardial effusion. Moderate to large effusions, determined at echocardiography as being more than 10 mm separation of the pericardial layers during diastole, should be drained before any elective surgery takes place. Haemodynamic effects of the effusion should be assessed via echocardiographic studies and quantified prior to induction of anaesthesia as detailed below.

#### **3.4 Pericardial effusions and tamponade**

Pericardial effusion occurs when there is excessive fluid accumulation within the pericardial space [3–10, 12, 17–41]. The effusion may be transudative, exudative, haemorrhagic or purulent depending on the cause. Progressive accumulation of fluid within the pericardial sac may lead to compression of cardiac chambers, obstruction of cardiac filling and tamponade.
