Cardiology
Question 172 of 180
A 43 year old woman presents to the Emergency Department with a 2 day history of chest pain. She describes a gradual onset of a sharp, central pain. She describes the pain as worse on coughing and radiating to the neck and left shoulder. She denies shortness of breath. She has no significant past medical history. On examination you note normal and equal breath sounds. You find the heart sounds to be normal although quiet. What is the most likely diagnosis?
Answer:
- Symptoms:
- The key finding on history is a constant, pleuritic central chest pain that is worse on coughing or lying supine and relieved when sitting up or leaning forwards, and that radiates to one or both trapezius ridges (phrenic nerves both innervate the pericardium and trapezius ridges).
- A prodrome of myalgias and malaise may be present with any cause of acute pericarditis, particularly in young adults.
- The presence of associated high or spiking fever suggests an infectious cause.
- Signs:
- The presence of a pericardial friction rub on physical examination is the key finding that supports the diagnosis; it is best at the left lower sternal border with the patient leaning forward at end-expiration
- Distant heart sounds with a quiet precordium is a common finding in pericardial effusion.
Pericarditis
Cardiology
Last Updated: 8th September 2021
Pericarditis is an inflammation of the pericardium. The acute form is defined as new-onset inflammation lasting < 4-6 weeks. It can be either fibrinous (dry) or effusive with a purulent, serous, or haemorrhagic exudate. It is characterised clinically by a triad of chest pain, pericardial friction rub, and serial electrocardiographic changes. Acute pericarditis is more common in adults (typically between 20 to 50 years old) and in men.
Causes
- Common causes:
- Idiopathic
- Viral infections e.g. coxsackievirus, echovirus, mumps, Epstein-Barr virus, cytomegalovirus, varicella, rubella, HIV, Parvovirus B19)
- Systemic autoimmune disorders (e.g. SLE, rheumatoid arthritis, systemic sclerosis, reactive arthritis, familial Mediterranean fever, systemic vasculitides, inflammatory bowel disease)
- Less common causes:
- Bacterial/fungal/parasitic infections
- Secondary immune processes (e.g. rheumatic fever, postcardiotomy syndrome, post-MI syndrome)
- Pericarditis and pericardial effusions in diseases of surrounding organs (e.g. acute MI, myocarditis, paraneoplastic syndromes)
- Metabolic disorders (e.g. uraemia, myxoedema)
- Post-surgery, radiotherapy or trauma
- Malignancy
- Drug related e.g. hydralazine, procainamide, isoniazid, chemotherapy drugs
Clinical features
Acute pericarditis is a clinical diagnosis. Aspects of the clinical history and presentation, physical examination, and ECG need to be combined in order to make the diagnosis. The diagnosis is confirmed in the presence of at least 2 of the 4 clinical criteria: typical chest pain, pericardial friction rub, widespread ST elevation, and pericardial effusion.
- Symptoms:
- The key finding on history is a constant, pleuritic central chest pain that is worse on coughing or lying supine and relieved when sitting up or leaning forwards, and that radiates to one or both trapezius ridges (phrenic nerves both innervate the pericardium and trapezius ridges).
- A prodrome of myalgias and malaise may be present with any cause of acute pericarditis, particularly in young adults.
- The presence of associated high or spiking fever suggests an infectious cause.
- Signs:
- The presence of a pericardial friction rub on physical examination is the key finding that supports the diagnosis; it is best at the left lower sternal border with the patient leaning forward at end-expiration
- Distant heart sounds with a quiet precordium is a common finding in pericardial effusion.
- ECG findings:
- The classic ECG changes are global upwardly concave ST-segment (J-point) elevations with PR segment depressions in most leads with J-point depression and PR elevation in leads aVR and V1. If the patient is seen soon after symptom onset, PR depressions may be noted prior to ST elevation.
- The ECG may evolve over 4 phases: stage 1 consists of ST elevation and upright T-waves that may resolve to normal (stage 2) over a period of several days or evolves further to T-wave inversion (stage 3) and then to normal (stage 4).
- Other tests:
- FBC: leucocytosis with a marked shift to the left may be seen with purulent pericarditis or other infectious aetiology
- Urea: elevated levels of urea (particularly >21.4 mmol/L) suggest a uraemic cause
- ESR/CRP: elevated ESR/CRP is consistent with an inflammatory state
- Initial and serial serum troponins: elevated levels may be present and reflect myocardial involvement, but the test is not specific or sensitive
- Chest x-ray: often normal unless there is an associated large pericardial effusion, in which a water bottle-shaped enlarged cardiac silhouette with a distinct pericardial fat stripe is seen; may also demonstrate concomitant lung pathology providing evidence of tuberculosis, fungal disease, pneumonia, or a neoplasm that may be related to the disease
- Pericardiocentesis: purulent pericarditis is immediately life-threatening and requires immediate confirmation of diagnosis via urgent pericardiocentesis; pericardial fluid should be tested for bacterial, fungal, and tuberculous causes, and blood should be drawn for culture
- Echocardiography: indicated to detect complications such as pericardial effusion, especially when cardiac tamponade is suspected, and can also help differentiate pericarditis from acute coronary syndromes; global ST elevations in the absence of left ventricular (LV) wall motion abnormalities and a pericardial effusion support the diagnosis of acute pericarditis
- Chest CT: can help diagnose constrictive pericarditis or pericardial effusion
Differential diagnosis
- Myocardial infarction or ischaemia
- Pulmonary embolism
- Pneumonia
- Pneumothorax
- Costochondritis
Management
Treatment is directed at any identified underlying disorder with supportive management directed at relief of symptoms. Hospitalisation is generally recommended to determine aetiology, observe for complications such as cardiac tamponade, and gauge response to therapy.
- Pericardial effusion
- Accumulation of transudate, exudate, or blood in the pericardial sac can occur due to pericardial inflammation. If a pericardial effusion is present, pericardiocentesis is indicated for clinical tamponade, for high suspicion of purulent or neoplastic pericarditis, or if the effusion is large or symptomatic. The effusion should be drained dry and the fluid analysed for glucose, protein, and lactate dehydrogenase. Cell count, microscopy, bacterial and/or viral culture, and cytological examination should be performed.
- In the absence of these indications, medical therapy is started as dictated by the cause.
- Purulent pericarditis
- If purulent pericarditis is suspected, urgent percutaneous pericardiocentesis with rinsing of the pericardial cavity and intravenous antibiotics are mandatory. Initial empiric antibiotic treatment comprises an anti-staphylococcal antibiotic plus an aminoglycoside, with later tailoring of antibiotics depending on underlying pathogens identified from pericardial fluid and blood cultures. Therapy with systemic antibiotics should be continued until fever and clinical signs of infection have resolved.
- An NSAID should also be started immediately on diagnosis for symptom management and continued for 4 weeks with a proton-pump inhibitor to reduce gastrointestinal adverse effects.
- Open surgical drainage via a subxiphoid pericardectomy may also be required. Pericardectomy in these patients is necessary in the presence of dense adhesions or loculations, persistent bacteraemia, recurrent tamponade, or progression to constrictive physiology.
- Non-purulent pericarditis
- NSAIDs are given for symptom relief. They reduce fever, chest pain, and inflammation but do not prevent tamponade, constriction, or recurrent pericarditis. NSAIDs are given first line for 4 weeks with a proton-pump inhibitor to decrease the risk of gastrointestinal adverse effects . Colchicine is recommended as a first-line adjunct therapy to NSAIDs as it improves response, decreases recurrences, and increases remission rates. It is given for 3 months in this setting.
- In cases of idiopathic or viral pericarditis, if chest pain has not resolved after 2 weeks, a corticosteroid can be considered as an option in patients who do not respond to anti-inflammatory therapy, or for patients in whom an NSAID is contraindicated, once an infectious cause has been excluded (corticosteroids are not recommended in patients with viral pericarditis because of the risk of reactivation of the viral infection and ongoing inflammation). They may also be used when there is a specific indication for their use (e.g., the presence of an autoimmune disease).
- In addition to the above treatment, the underlying cause should also be treated if known:
- In patients with tuberculous pericarditis, first-line treatment is 4 to 6 weeks of anti-tuberculous therapy.
- Most patients with uraemic pericarditis respond to intensive dialysis within 1 to 2 weeks.
- Autoimmune disorders are treated with corticosteroids and/or other immunosuppressive therapies depending on the specific condition.
- Treatment of neoplasms may involve any combination of radiotherapy, chemotherapy, or surgery, depending on the type of tumour identified.
- Patients with viral pericarditis may benefit from specific antiviral therapy.
Complications
- Pericardial effusion with cardiac tamponade
- Increased intrapericardial pressure from the pericardial effusion can compress the cardiac chambers limiting cardiac filling. The clinical presentation and the haemodynamic effect of cardiac tamponade depend on the size of the pericardial effusion, the time over which the fluid accumulated, and the clinical circumstances. When pericardial fluid accumulates rapidly, impaired cardiac filling quickly progresses to cardiogenic shock followed by pulseless electrical activity.
- Symptoms include dyspnoea and chest pain. Examination findings suggestive of cardiac tamponade include tachycardia, tachypnoea, hypotension, elevated jugular venous pressure, distended neck veins, Kussmaul's sign (a rise in venous pressure with inspiration) and pulsus paradoxus. ECG may show low QRS voltages and electrical alternans (alternating QRS amplitude in any lead, caused by the heart swinging in the pericardial sac).
- Urgent echocardiography is indicated to establish the effusion size, location, and haemodynamic effect. The treatment of tamponade is emergency drainage of the pericardial fluid using needle pericardiocentesis. Pericardiocentesis is performed under echocardiographic guidance. Surgical drainage may be indicated in cases of haemopericardium due to trauma, type A aortic dissection, or ventricular free wall rupture following myocardial infarction.
- Chronic constrictive pericarditis
- In the healing process of acute, fibrinous, serofibrinous, or chronic pericardial effusion, the pericardial cavity can be completely replaced by granulation tissue. This results in a dense scar that encases the heart and interferes with ventricular filling.
- Constrictive pericarditis should be suspected in a patient with unexplained right heart failure in whom there is a history of pericardial disease or predisposing pericardial injury even if the pericardial insult predates the clinical presentation by years. Symptoms and signs of right-sided heart failure include fatigue, ankle oedema and, in, severe cases, ascites.
- Most cases occur within 3 to 12 months after the pericardial insult. It is a relatively rare complication and in developed countries is most frequently caused by prior cardiac surgery, radiotherapy, and idiopathic pericarditis.
- Surgical pericardial resection is the definitive treatment.
Report A Problem
Is there something wrong with this question? Let us know and we’ll fix it as soon as possible.
Loading Form...
- Biochemistry
- Blood Gases
- Haematology
| Biochemistry | Normal Value |
|---|---|
| Sodium | 135 – 145 mmol/l |
| Potassium | 3.0 – 4.5 mmol/l |
| Urea | 2.5 – 7.5 mmol/l |
| Glucose | 3.5 – 5.0 mmol/l |
| Creatinine | 35 – 135 μmol/l |
| Alanine Aminotransferase (ALT) | 5 – 35 U/l |
| Gamma-glutamyl Transferase (GGT) | < 65 U/l |
| Alkaline Phosphatase (ALP) | 30 – 135 U/l |
| Aspartate Aminotransferase (AST) | < 40 U/l |
| Total Protein | 60 – 80 g/l |
| Albumin | 35 – 50 g/l |
| Globulin | 2.4 – 3.5 g/dl |
| Amylase | < 70 U/l |
| Total Bilirubin | 3 – 17 μmol/l |
| Calcium | 2.1 – 2.5 mmol/l |
| Chloride | 95 – 105 mmol/l |
| Phosphate | 0.8 – 1.4 mmol/l |
| Haematology | Normal Value |
|---|---|
| Haemoglobin | 11.5 – 16.6 g/dl |
| White Blood Cells | 4.0 – 11.0 x 109/l |
| Platelets | 150 – 450 x 109/l |
| MCV | 80 – 96 fl |
| MCHC | 32 – 36 g/dl |
| Neutrophils | 2.0 – 7.5 x 109/l |
| Lymphocytes | 1.5 – 4.0 x 109/l |
| Monocytes | 0.3 – 1.0 x 109/l |
| Eosinophils | 0.1 – 0.5 x 109/l |
| Basophils | < 0.2 x 109/l |
| Reticulocytes | < 2% |
| Haematocrit | 0.35 – 0.49 |
| Red Cell Distribution Width | 11 – 15% |
| Blood Gases | Normal Value |
|---|---|
| pH | 7.35 – 7.45 |
| pO2 | 11 – 14 kPa |
| pCO2 | 4.5 – 6.0 kPa |
| Base Excess | -2 – +2 mmol/l |
| Bicarbonate | 24 – 30 mmol/l |
| Lactate | < 2 mmol/l |
