Key facts:
Authors: Liam Linney, Alison Hewitt, Yukki Wong, Dawn Adamson
Top Tip: Consider secondary, as well as primary causes
Key Differential Diagnoses
- Viral infection (not serious to miss)
- Myocardial infarction (very serious to miss)
- Myocarditis
- Pleuritic chest pain, causes of (eg PE, pneumonia)
Key Investigations
- ECG, CXR
- Troponin I (6h) + Troponin T (12h)
- U+E, Glucose, LFT, Bone
- FBC, ESR, CRP
- ± BC, ECHO
- ± Viral serology (rarely affects Mx)
Key Treatment
- Treat the cause
- ± PO PARACETAMOL 1g tds
Key Management Decision
- Pericardiocentesis (only if significant effusion)
Background
The commonest causes are: viral, idiopathic and post-MI. But think about more serious causes
Introduction
- Acute pericarditis is a common disease that should be considered in the differential diagnosis of all adults presenting with chest pain. But it is a diagnosis of exclusion; after MI etc have been excluded
- There is normally less than 50 mls of fluid in the pericardial space. It is an acute inflammation of the pericardium, usually without an associated pericardial effusion; and can occur as an isolated clinical problem or as a manifestation of systemic diseases
- Usually the pericardium becomes acutely inflammed, with pericardial vascularisation and infiltration with polymorphonuclear leucocytes. A fibrinous reaction frequently results in exudate and adhesions within the pericardial sac and a serous or haemorrhagic effusion may develop. In some conditions (TB, sarcoid, fungal infections and rheumatoid arthritis) a granulomatous pericarditis develops
- Pain is similar to pleuritic. But pericarditis is positional and pain is worse on leaning forwards. Pleurisy is usually not positional
- 20% have a pericardial friction rub, which is the characteristic sign. It can be missed easily, if soft, or if you do not lean the patient forward
- Pleuropericarditis exists, ie patient can get similar pain from both serous membranes. Pericardial effusion and cardiac tamponade are rare; both often missed, as symptoms are non-specific - and signs of tamponade overlap with RHF (JVP is usually increased and there may be peripheral oedema, and lung fields are usually clear)
- Myopericarditis also exists. Raised troponins can suggest this diagnosis
Note: remember ST elevation and Troponin T/I rise can occur in both; and acute pericarditis can complicate MI
Definition
- Acute inflammation of the pericardium
Causes
There are three common causes:
- Viral - particularly coxsackie viruses
- Idiopathic
- Post-MI (5% of patients; days 2-4)
Other causes include:
- PE/pulmonary infarction
- Dressler's syndrome (2wks - 2mths after MI (3%), or cardiac surgery)
- Infective; other viruses (eg Mumps, influenza, HIV, varicella); bacterial (rheumatic fever, pneumonia, septicaemia, TB (note: untreated TB has 85% mortality), fungi
- CRF (severe) ie 'uraemic'
- Metabolic/endocrine: hypothyroidism, hyperuricaemia
- Trauma
- Connective tissue disorders - systemic lupus erythematosus, rheumatoid arthritis, vasculitis
- Cancer invading the pericardium - breast, bronchus or lymphoma
- Drugs: procainamide, hydralazine, minoxidil, methyldopa, isoniazid, rifampicin, penicillin
- Rare causes: granulomatous disease (eg sarcoid), endomyocardial fibrosis, radiotherapy, post-cardiotomy syndrome
Symptoms
- Chest pain (rapid-onset, worse on inspiration, coughing or lying down; relieved by leaning forward; may be referred to L shoulder if diaphragm is affected). Pain can also be intermittent and positional. Pleuritic pain can be similar but is not usually positional. SOB is occasional feature
- Fever
Note: pleuritic chest pain has same features; can have both in pleuropericarditis - Of pericardial effusion (SOB)
- Of cardiac tamponade (dizziness secondary to low BP, symptoms of shock)
Key questions
- "When did the chest pain start?"
- "Is it worse when you breath in, move or cough?"
- "Is it worse when you change body position?"
- "Have you had a temperature or a cough?"
Signs
- May be none
- Fever
- Pericardial friction rub: 20% of patients; scratchy noise, in time with heart beat, but louder on inspiration; often maximal at lower LSE, increased by leaning forward. The last three characteristics are also features of the murmur of aortic regurgitation. Can also be confused with MT/TR due to its position. The rub can also be intermittent, positional and elusive. So examine every day
- Of pericardial effusion (raised JVP and signs of RHF; lung fields are usually clear)
- Of cardiac tamponade: tachycardia, hypotension, pulsus paradoxus (= increase in normal decrease in pulse volume on inspiration; >15 mmHg fall systolic BP, on inspiration)
- Note: the paradox is that heart continues to best strongly despite arterial pulse virtually disappearing
- This is done by taking the BP, but slowly. Initially the heart sounds will be intermittent. As the cuff is deflated, the heart sounds will eventually become continuous
- The difference is the amount of pulsus paradoxus
- Other signs include:
- Kussmaul's Sign (rise in JVP on inspiration, usually falls)
- Difficult to feel apex
- Faint heart sounds
Beck's Triad
Becks Triad = hypotension, muffled heart sounds, raised JVP. This was described by cardiac surgeon Claude Beck. If all three of this trio are present, it is considered pathognomic for cardiac tamponade.
The trio can easily be remembered using three D’s:
- Decreased arterial pressure
- Distended neck veins
- Distant heart sounds
Sternbach G. "Claude Beck: cardiac compression triads". J Emerg Med 1988; 6(5): 417–9
Investigation
A rise in Troponin T/I can occur - due to an associated myocarditis (ie myopericarditis). So Trop T can be a bad prognostic marker; myopericarditis can progress to a fulminant myocarditis
Blood
- FBC, ESR, CRP
- U+E, Glucose, LFT, Bone
- Troponin I (6h) + Troponin T (12h)
± Viral serology (acute and 2/52 later); rarely affect Mx
± BC, fungal precipitins (if indicated)
± TFTs
Other
- ECG: characteristic finding = concave ('saddle-shaped') ST elevation (vs convex in MI) in most (vs a territory in MI) leads without reciprocal ST depression (unlike MI); in at least 2 limb leads and V3-6
- PR depression (rare in MI); T waves initially peaked, then flattened or inverted; pathological Q waves do not occur
- SR is usual, but AF, atrial flutter and atrial ectopics occur
- In pericardial effusion/tamponade: low-voltage complexes, or alternating ECG morphology (electrical alternans)
- CXR: normal (unless pericardial effusion, when may show globular heart)
Notes: mainly done to exclude other diagnoses eg pneumonia, PE, pneumothorax - ± Pericardiocentesis (diagnostic, or to obtain MB data); with ECG/ECHO monitoring, with surgical backup; particularly important in suspected purulent pericarditis, to isolate the organism, which will guide AB Rx
CXR (pleural effusion)
- An enlarged flask-shaped cardiac silhouette may be the first sign of a large pericardial effusion. This may not be evident in patients with small effusions (less than a few hundred mls), who may present with a normal cardiac silhouette
- In one study, pleural effusions were seen in 33% of patients. Approximately 75% of the effusions were left-sided only
Diagnosis
- History, examination, and ECG (and MI excluded)
Key Investigation
- ECG
Specialist Investigation
- ECHO; not normally necessary (unless pericardial effusion/tamponade suspected)
Differential Diagnosis
- Viral infection
- Myocardial infarction
- Myocarditis (this causes LV impairment)
- Pleuritic chest pain, causes of (eg PE, pneumonia, pneumothorax
- Myopericarditi
- Musculoskeletal
- GI causes
- Rheumatic fever (now rare)
Treatment
Treat the Cause: eg Immunosuppression in SLE, remove drug if drug cause
Treatment (first line)
Drugs
- PO PARACETAMOL 1g tds ± opiate
Note: pain relief is main treatment. Can often do nothing about the most common underlying cause ie virus. Analgesia of choice is now simple analgesia, eg paracetamol. NSAIDS can increase infarct size and may depress myocardial function - ± Antibiotics, or Anti-TB Rx
Procedures
- IV line
Stop
- Drugs if thought to be cause; ENOXAPARIN/WARFARIN (may precipitate bleed into pericardium)
Treatment (second line)
Drugs (mainly for chronic or recurrent pericarditis)
- PO COLCHICINE 1mg stat, then 0.5 mg qds, 48 hrs: [Ref]
- ± PO PREDNISOLONE 40-60 mg od, for upto 2 wks
Procedures
- Pericardiocentesis (if tamponade, and systolic BP
Prescribing issues
- NSAIDs contraindicated - if MI, myocarditis or bleeding (malignancy, trauma)
Key management decision
- Pericardiocentesis; diagnosis, treatment (tamponade)
Admit?
- Many can be managed as outpatients. Admit if unwell, cardiac enzymes raised, or concern re tamponade
Bed plan
- Medical Admission Ward, or CCU
Referrals
- Cardiology
The Rest
Complications
- Pericardial effusion, cardiac tamponade, constrictive pericarditis
- AF/Atrial flutter
- Recurrent or chronic pericarditis (rare)
Follow-up
- Cardiology; 2/52 to repeat viral serology, if necessary
Prognosis
- The prognosis for people who have pericarditis depends on the cause. When pericarditis is caused by a virus or when the cause is not apparent, recovery usually takes 1 to 3 weeks. Complications or recurrences can slow recovery
- People with cancer that has invaded the pericardium rarely survive beyond 12 to 18 months. [Ref]
Risk stratification
- Usually safe to be discharged at 24-48h, if well, and no obvious serious cause; some mild cases can be managed as an OP: [Ref] .
2° Prevention
+ Health promotion
- Post-infarct pericarditis usually appears by day 2. Therefore is would be unusual for it to develop after discharge
- Dressler’s syndrome develops 2-10 weeks post MI. Warning about it may be helpful
Don't forget
- Put a venflon in ASAP (in case, it is an MI)
- To exclude MI (ST elevation and Troponin T rise can occur, in both)
- Send off viral serology
- Untreated TB has 85% mortality; but is very rare
Red flags
- Pericardial effusion
- Tamponade
- RHF/CCF
- Cardiogenic shock
