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Pericarditis and Cardiac Tamponade - 2/1/2013

posted Feb 1, 2013, 10:56 AM by Rohit Das   [ updated Feb 1, 2013, 11:12 AM by Purnema Madahar ]

Pericarditis is a fairly uncommon cause of acute chest pain, representing 5-7% of such presentations to the ED in one series. Though generally a benign process, up to 10% of cases (and a higher incidence with certain etiologies) can lead to cardiac tamponade, a complication associated with a high mortality rate. At Chief of Service today, we discussed a case of a young woman presenting with pericarditis and  consequent tamponade, in the context of a known history of SLE and stage IV cervical cancer, all complicated by the fact that she was also on LMWH for antiphospholipid syndrome…ultimately, cytology was positive for malignant cells, a very surprising finding indeed…

·         Quick overview on pericarditis – what are the causes and how is it diagnosed?

·         What etiologies are pertinent to this patient’s differential?

·         What are the clinical and echocardiographic signs of cardiac tamponade?

·         What is the management of pericarditis? Did anticoagulation play a role in this patient’s decompensation?

 

Quick overview on pericarditis – what are the causes and how is it diagnosed?

·         Anatomically, the pericardium has two layers – the visceral pericardium (adherent to the myocardium) and the more fibrous parietal pericardium. Normally, there is about 1-2mm of space between these two layers, and the pericardial sac contains 15-35cc of fluid. Physiologically, the purpose of the pericardium is to protect the heart, limit chamber dilatation (mainly of the thin walled right atrium and right ventricle) and equalizes compliance between the left and right ventricle.

·         Inflammation of the pericardium, i.e. pericarditis, has too many causes to list – for a good synopsis, please see the table on page 2 of the attached Lancet review. The most common identifiable cause is viral and the cause remains unidentified in up to 20-30% of cases.

·        Pericarditis is mainly a clinical diagnosis requiring two of the four following characteristics – typical chest pain, a pericardial rub, consistent EKG changes, and the presence of a new or worsening pericardial effusion.

o   The chest pain of pericarditis is typically progressive, severe, pleuritic, and worse when supine, while relieved with sitting.

o   Pericardial rub is often a transient heart sound, but is pathognomonic for pericarditis. It is best heard at the left sternal border, with the patient sitting upright, holding their breath in deep expiration. The sound is often likened to two pieces of sandpaper rubbing against each other; half of patients will have a “triple cadence” with one sound heard in systole and the other two in diastole, though most will have one or two components to the rub.

o   The classic EKG shows widespread “saddle-shaped” ST elevations that may be accompanied with PR depressions. Typically, T waves are upright initially, and become inverted after normalization of ST elevations – this is a key differentiating factor from ischemic ECG findings.

o   Effusion is diagnosed mainly by imaging - >250cc of fluid can be seen accurately on chest radiography, and otherwise TTE provides definitive testing. Effusion is not always present with pericardial inflammation, so its absence definitely does NOT rule out the diagnosis.

·      Since the course of pericarditis is generally benign and extensive evaluation reveals a cause in only a minority of patients, an effort to find the cause in all patients is not recommended. Rather, evaluation should focus on identifying a significant effusion and etiologies that require specific therapy (e.g., TB, malignancy or purulent disease).

 

What etiologies are pertinent to this patient’s differential?

Want to focus here on SLE-related pericardial disease, and malignancy.

·    There are several cardiac manifestations of SLE, including coronary artery disease (with multiple different mechanisms contributing, including accelerated atherosclerosis), pericarditis, valvular abnormalities, and myocarditis. Pericarditis is by far the most common NON-coronary manifestation, and some degree of pericardial abnormality is found on TTE in 11-50% of SLE patients. Most patients are asymptomatic, and for those who do have symptoms, the course is generally benign and very rarely leads to complicated pericardial disease…

·         Malignancy is not a common cause of pericarditis, but of the potential causes, is probably most commonly associated with complicated disease and hemorrhagic pericardial effusions in the developed world (otherwise TB predominates) – in one series of symptomatic pericardial effusions, almost half were due to malignancy. The most common etiologic cancer is lung tumors, but other common etiologies include breast, esophageal, lymphoma and melanoma among others…cervical cancer, from what I can gather, is a very INFREQUENT cause – the literature is limited to about 6-7 case reports, one of which cites a 0.3 to 3.2% prevalence of cardiac metastasis at autopsy…

 

What are the clinical and echocardiographic signs of cardiac tamponade?

Tamponade occurs when an effusion becomes large enough to generate intrapericardial pressures that exceed diastolic filling pressures, thus impairing ventricular filling.

·     The main clinical signs of tamponade are elevated jugular veins (100% of patients), tachycardia (80-100%) and pulsus paradoxus (an abnormally high inspiratory fall in systolic BP, which is physically normal up to a degree…) of greater than 10mmHg (98% of patients). At a threshold of 12mmHg, the pulsus paradoxus is a very accurate test on both sides of the coin, with a +LR of around 6, and a –LR of 0.03.

·         Echocardiogram is also very helpful in assessing for tamponade physiology. The three major findings are right-sided diastolic collapse, substantially increased respiratory variation in transmitral and transtricuspid flow, and IVC plethora (dilatation and less than 50% reduction of IVC diameter during inspiration).

 

What is the management of pericarditis? Did anticoagulation play a role in this patient’s decompensation?

·         Pericarditis is generally benign and treated supportively with anti-inflammatory agents – high dose ASA and NSAIDs (Ibuprofen preferred). Colchicine can be useful as an adjunct to NSAIDs for initial cases of pericarditis, but it is the agent of choice for recurrent cases (which occurs 30% of the time). Steroids should be avoided due to the theoretical increased risk of recurrent disease, but can be considered for refractory cases, cases due to TB (since it has been shown to prevent progression to constrictive physiology) and pericarditis due to a systemic inflammatory illness. Surgical drainage is indicated for clinical tamponade, purulent pericarditis, and when suspicion for malignancy or TB related pericardial disease is high.

·        One of the interesting aspects of this case was the concurrent use of LMWH in the context of pericardial inflammation. The conventional recommendation is to avoid anticoagulation due to the risk of hemorrhagic conversion and acute worsening of the effusion...

o   In the attached prognostic study, about 450 patients with acute pericarditis (specific cause identified in only 17%) were followed prospectively and assessed for complications (recurrence, tamponade or constrictive disease). The only adverse prognostic factors that remained significant after multivariate analysis were female gender, large effusion and failure of NSAID/ASA therapy. Overall, despite the theoretical risk, the poor prognostic implications of anticoagulation haven’t really borne out in the literature…

 

Very interesting case of metastatic cervical cancer leading to malignant pericarditis…hope someone writes it up one day...Attached is a review article on Pericarditis, a nice RCE piece on diagnosing cardiac tamponade, an overview of the cardiac manifestations of SLE and the prognostic study that I mentioned above…probably should digest all of it on an empty stomach…Have a good weekend!


Pericarditis
Troughton et. al., Lancet 2004, Volume 363: 717-27

Roy et. al., JAMA 2007, Volume 297: 1810-18

Doria et. al., Lupus 2005, Volume 14: 683-86

Imazio et. al., Circulation 2007, Volume 115: 2739-44
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