ACUTE PERICARDITIS

ACUTE PERICARDITIS

Course objective:

• Know how to recognize the main clinical signs of acute pericarditis.
• The principles of searching for an etiology on which the therapeutic attitude will depend.

1. Definition : 

• It is an acute inflammation of the pericardium with or without pericardial effusion. 

2. Anatomical reminder:

The pericardium is composed of

• Parietal pericardium: a solid, conical fibrous sac that contains the heart and the roots of the great vessels.
• Visceral pericardium or epicardium: serous membrane which covers the entire myocardium of the four cavities, of transparent thinness explaining the epicardial participation in myocardial lesions.
• A normally virtual cavity, between the two layers, all around the heart.
• The pericardial fluid normally remains in very small quantities (20 cm3). Clear, rock water, it appears as an ultrafiltrate of the plasma, with little protein (2 g%) and low osmotic pressure.

3. Diagnosis:

• It is based on the classic triad of pain, fever and electrocardiographic changes. 

ACUTE PERICARDITIS

1. Clinic:
   1. Functional signs:

• Precordial or retrosternal chest pain , often sudden and violent, sometimes simulating anginal pain but:
  • Long duration. Not sensitive to nitrates.
  • Increases with deep inspiration and coughing, even swallowing, hence dysphagia.
  • Radiates to the back, sometimes to the left supraclavicular region in a “strap” fashion 
  • Varies with position and relieved by leaning forward
  • Improved by anti-inflammatories
• Dyspnea is most often moderate, superficial polypnea type.
• Mediastinal signs: 
  • They are only seen in abundant pericardial effusions.
  • Hiccups and dysphagia.

2. General signs:

• Moderate fever with signs suggestive of a viral infection (nasopharyngitis, myalgia) in the preceding days.
• Other signs depending on the cause: weight loss, sweating, arthralgia, etc.

3. Physical signs:

• Make the diagnosis:
  • Pathognomonic but inconstant pericardial friction, producing a systolic-diastolic noise, superficial, mesocardial, localized not radiating, of variable intensity, fleeting, modified by the position and pressure of the stethoscope, persists during apnea, variable timbre.
  • Careful auscultations must be repeated.
  • Muffling of heart sounds at the tip.
  • Decrease in peak shock
  • Moderate tachycardia
• Look for signs of poor tolerance (see tamponade):
  • Right heart failure picture (hepatomegaly, RHJ)
  • Pulse, blood pressure
• Look for arguments of etiological orientation:
  • Lung examination looks for signs of pleural effusion.
  • Examination of the skin, ENT, joints, lymph node areas and breasts.

2. ECG:

• ECG signs are frequent, early and labile, hence the need to repeat the tracings, and mainly concern the ST segment and the T wave, the evolution is done in 4 Holzmann stages:
  • Stage I (<24h): ST segment elevation concave upwards.
  • Stage II (<48h): return of ST to the isoelectric line with flattening of T waves  
  • Stage III (<7 days): generalized T wave inversion  
  • Stage IV (<2 months): ECG returns to normal.
• A normal ECG does not rule out the diagnosis  

3. Chest X-ray:

• Normal X-ray in case of dry pericarditis.
• Abundant effusion:
  • Symmetrical cardiomegaly in a carafe or teapot.
  • Vascular pedicle widened and short.

ACUTE PERICARDITIS

4. Echocardiography:

It can allow you to:

• Highlight pericardial effusion:
  • Systolodiastolic detachment of the two layers of the pericardium in the form of an echo-free space between the epicardium and the pericardium. 

• Allows the effusion to be quantified approximately:
  • 2D mode allows to highlight the septate or encysted EPs
• Monitor the evolution.
• Look for signs of poor tolerance (see tamponade)
• Sometimes find arguments in favor of the etiological diagnosis.

5. Chest CT scan and MRI:

• Can easily demonstrate pericardial effusion.
• Are sometimes useful in the search for an etiology.

6. Biological tests:
   1. Systematic assessment: 

• NFS – grouping, hematocrit, platelets
• Plasma urea and creatinine, blood ionogram
• Blood sugar, Labstix
• VS, CRP, ASLO.
• IDR with tuberculin 10 iu.

2. Other examinations:

• Depending on the context 
• Viral serology
• T3, T4, TSHus
• Immunological tests.

7. Pericardial puncture/biopsy:

• It is sometimes guided by pericardioscopy or echocardiography.
• It allows histological, biochemical and PCR analysis of the liquid and to confirm the etiological diagnosis.
• Indications for pericardial puncture/biopsy:
  • Mandatory in case of emergency tamponade.
  • Abundant or recurring effusion.
  • Suspicion of tuberculous, purulent or neoplastic pericarditis.  
  • For diagnostic purposes if non-invasive tests are inconclusive.

4. Surgical drainage. 

Represents the emergency procedure in the event of pericardial tamponade.

5. Pericardial biopsy.

• The main interest of pericardium biopsy is to establish the etiology of the causal condition.

6. Differential diagnosis:

• In the face of chest pain:
  • Myocardial infarction
  • Pulmonary embolism
  • Aortic dissection 
  • Acute pneumonia…
• In front of cardiomegaly: cardiomyopathies

7. Etiologies:
   1. Acute idiopathic pericarditis:
      1. Diagnosis:

• It represents the most frequent etiology.
• A viral context could be found during the interrogation 
• Their evolution is most often spontaneously favorable, only very rarely evolving towards constriction and even more exceptionally towards tamponade.
• The particularity of these pericarditis is that they are recurrent.

2. Viral pericarditis:
   1. Diagnosis:

• Definite diagnosis of pericarditis can only be made by PCR analysis of pericardial fluid or tissue.
• An increase in serum antibodies in two samples taken one month apart is highly suggestive of the diagnosis.
• The viruses most often involved are: coxsackie B, CMV, influenza virus, infectious mononucleosis, adenovirus, enterovirus, echovirus.
• Their evolution is most often spontaneously favorable, only very rarely evolving towards constriction and even more exceptionally towards tamponade.

3. Tuberculous pericarditis:
   1. Diagnosis:

• It is a subacute pericarditis with abundant fluid. 
• It is rarely secondary to hematogenous spread of BK; it is a matter of close contamination or lymphogenous contamination. 
• The insidious clinical onset: Fever, deterioration of the general condition, chest pain may be absent.
• Sometimes an inaugural cardiac tamponade.
• The notion of tuberculosis should be sought in the entourage.
• Radiological pulmonary abnormalities are frequent (progressive or sequelae of tuberculous lesions). 
• The IDRt is positive (> 10 mm in the absence of a vaccination scar, > 15 mm if a vaccination scar). A negative IDRt does not rule out the diagnosis.
• Progression to constrictive pericarditis is common.

4. Purulent pericarditis: 

• The most serious etiology after pericardial cancers, with a mortality rate still exceeding 35%
• Any pericarditis of any origin (collagenosis, uremia, diabetes, myocardial infarction, etc.) can progress to purulence.
• The picture is much more torpid, dominated by fever and other general signs, with few elements drawing attention to the pericardium.
• The germs involved are most often Staphylococcus aureus and Gram-negative bacilli.

5. Neoplastic pericarditis:

• It may be a primary pericardial malignancy or secondary invasion of the metastatic pericardium .
• Most often hemorrhagic pericarditis with significant effusion, deterioration of general condition, signs of cardiac compression and sometimes tamponade. 

6. Pericarditis of chronic renal failure:

• The occurrence of acute pericarditis in this setting represents an indication for emergency purification, which can reverse the exudation .
• Treatment is based on an increase in the frequency and duration of dialysis.

7. Post-traumatic pericarditis:

• Blunt chest trauma: can cause very serious immediate hemopericardium, 

ACUTE PERICARDITIS

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ACUTE PERICARDITIS