Postpericardiotomy syndrome

Postpericardiotomy syndrome
Classification and external resources
ICD-9-CM 429.4
eMedicine article/891471

Postpericardiotomy syndrome (PPS) is a medical syndrome referring to an immune phenomenon that occurs days to months (usually 1–6 weeks[1]) after surgical incision of the pericardium (membranes encapsulating the human heart).[2] PPS can also be caused after a trauma, a puncture of the cardiac or pleural structures (such as a bullet or stab wound), after percutaneous coronary intervention (such as stent placement after a myocardial infarction or heart attack), or due to pacemaker or pacemaker wire placement.[1]

Signs and symptoms

The typical signs of post-pericartiotomy syndrome include fever, pleuritis (with possible pleural effusion), pericarditis (with possible pericardial effusion), occasional but rare pulmonary infiltrates, and fatigue.[1][2] Cough, pleuritic or retrosternal chest pain, joint pain and decreased oxygen saturation can also be seen in some cases.[1] One problem with this definition is that it is so non specific.

Physical findings

During medical doctor examination,a pericardial friction rub can be auscultated indicating pericarditis. Auscultation of the lungs can show crackles indicating pulmonary infiltration, and there can be retrosternal/pleuritic chest pain worse on inspiration (breathing in). Patient can also depict sweating (diaphoresis) and agitation or anxiety.

Radiological findings

A chest X-ray might depict pleural effusion, pulmonary infiltration, or pericardial effusion.[2]

Pathogenesis (Disease process)

This condition is a febrile illness caused by immune attack of the pleura and the pericardium. Possible cell mediated immunity led by Helper T-cells and Cytotoxic T-cells is postulated to be important in the pathogenesis of this condition.[1] There is also possibility of anti-cardiac antibodies created idiopathically, or due to concurrent cross-reactivity of the antibodies produced against viral antigens, however the latter assumption is not fool-proof or completely reliable due to conflicting studies.[1] It is entirely possible the autoimmune etiology is an ephiphenomenon and there is a more simple, more likely explanation like the impact of retained blood complications.

Epidemiology

Uncommon in children and often common in patients receiving cardiac operations that involves opening the pericardium.[1] CABG surgery is a common culprit.

Complications

Complications include pericarditis, pericardial effusion, pericardial tamponade, pleuritis, and pulmonary infiltration. Of these cardiac tamponade is the most life-threatening complication. The pericardial fluid increases intra-pericardial pressure therefore preventing complete expansion of the atria and the ventricles upon the diastole. This causes equilibration of the pressure in all four heart chambers, and results in the common findings of the tamponade which are pulsus paradoxus, Beck's triad of hypotension, muffled heart sounds, and JVD, as well as EKG or Holter monitor findings such as electrical alternans. Physically the patients who progress to severe pericardial tamponade obtundate, become mentally altered, and lethargic. If left untreated, severe cardiac output decrease, vascular collapse, and hypoperfusion of body including the brain results in death.

Prevention

It has long been taught that avoidance of injurious procedures is the only sure way to avoid this syndrome, however PPS by itself it not an indication of the quality of an operation. The mere opening of the pericardium in any form of cardiac operation is enough to cause this syndrome. However, its impossible to do an open operation on the heart without incising the pericardium. It may be best, looking forward, to more carefully study the potential etiologies (given the controversy around the autoimmune cause) to better figure out ways to prevent this common complication. Given that retained blood complications may be part of the etiology, examining ways to prevent common complications such as chest tube clogging may be a beneficial avenue to explore.

Colchicine treatment

Colchicine has been used effectively to prevent pericarditis, and inflammation that follows surgery of the pericardium.[3] Although no current drug on the market prevents post-pericardiotomy syndrome, colchicine seems to provide an effective and safe way to treat pericarditis by reducing inflammation.[4] Colchicine is a natural product extracted from plants, and is a secondary metabolite (an organic compound not directly related to growth and development in an organism).[3]

Colchicine interferes with the inflammatory process by altering several important steps in the pathway. Microtubules are structural components of the cytoskeleton that lengthen and shrink for important cell functions. Colchicine binds to β- tubulin and forms tubulin-colchicine complexes.,[3][4] These complexes interfere with microtubule formation microtubules. Low doses of colchicine can inhibit the formation of microtubules, while high doses depolymerize or break down a polymer to a monomer.[5] Therefore, any process involving cytoskeleton change, including mitosis and motility of white blood cells, are highly impacted.

Microtubule disruption decrease neutrophil adhesion, an important step for inflammation.[5] Neutrophils are recruited to the target location of inflammation via signals from the endothelium where they adhere and play a role in the inflammatory response. Colchicine diminishes neutrophil adhesion by decreasing expression of selectins, a family of cell adhesion molecules.[5] In addition, colchicine prevents the movement and secretion of intercellular granules, substances, proinflammatory enzymes from neutrophils, thus making a significant impact on inflammatory processes within the body.[4] The high concentration of colchicine in neutrophils, sixteen times greater compared the plasma levels, can account for the positive therapeutic effects.[4]

Many mediators are altered to assist neutrophils during inflammation, including the monokine tumor necrosis factor-alpha (TNFα).[6] Cytokines help stimulate the acute phase reaction in response to inflammation. Colchicine inhibits macrophage production of TNFα, leading to the interference between TNFα and neutrophil interaction.[6] There are many more effects of colchicine that are currently under research, and some aspects of this metabolite are not fully understood.

There was great hope that Colchicine could be a primary preventative measure in treating Post-Pericardiotomy Syndrome due to its anti-inflammatory effects.[4] In the COPPS-2 trial, however, perioperative use of colchicine compared with placebo reduced the incidence of postpericardiotomy syndrome but not of postoperative AF or postoperative pericardial/pleural effusion. The increased risk of gastrointestinal adverse effects reduced the potential benefits of colchicine in this setting. Thus colchicine is not likely going to be the ideal way to prevent this problem. [7]

References

  1. 1 2 3 4 5 6 7 M. Silvana Horenstein (April 30, 2009). "Postpericardiotomy syndrome". eMedicine from WebMD.
  2. 1 2 3 Marc. E. Kaminsky, Rodan B., Osborn D., Chen J., Sealy W., Putman C. "Postcardiotomy syndrome" (PDF). American Journal of Roentgenology.
  3. 1 2 3 Eur Heart, J. (2009). Colchicine for pericarditis: hype or hope? Oxford Journal. Vol 30. 532-539.
  4. 1 2 3 4 5 Eur Heart, J. (2010) Colchicine for the Prevention of the Post-pericardiotomy Syndrome (COPPS): a multiculture, randomized, souble-blind, placebo controlled trial. Oxford Journal. Vol 31. 2749-2754.
  5. 1 2 3 Spyridon Deftereos, S., Giannopoulos, G., Papoutsidakis, N., Panagopoulou, V., Kossyvakis, C., Raisakis, K., Stefanadis, C. (2013). Colchicine and the heart. Journal of the American College of Cardiology. Vol 62(20), 1817-1825.
  6. 1 2 Molad, Y. (2002). Update on Colchicine and Its Mechanism of Action. Current Rheumatology Reports. Vol 4. 252-256.
  7. ↑ "Colchicine for Prevention of Postpericardiotomy Syndrome and Postoperative Atrial Fibrillation. The COPPS-2 Randomized Clinical Trial". JAMA 312 (10): 1016–1023. 2014. doi:10.1001/jama.2014.11026.
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