Acute Pericarditis

The Scope

  • Visceral and Parietal layers of the pericardium – in between these layers is the pericardial space
  • Typically, there is up to 50mL of fluid in the space
  • On autopsy, 1 – 6 % of people have evidence of pericarditis
  • Up to 5% of patients that complain of chest pain, but do NOT have MI, may have pericarditis

The Causes

  • 90% – idiopathic or viral
  • 10% other: bacterial infection, tuberculosis, post-MI (often transmural), secondary to aortic dissection (if blood leaks into the pericardium), blunt or sharp chest trauma, neoplastic invasion, radiation exposure, uremia, post-thoracotomy, auto-immune, drug reaction
  • With the advent of coronary reperfusion, post-MI pericarditis is less common
  • Autoinflammatory disorders: Tumor necrosis factor Receptor–Associated Periodic Syndrome (TRAPS) and familial Mediterranean fever can cause repeated bouts of pericarditis

The Consequences

  • Cardiac Tamponade
  • Constrictive Pericarditis
  • Recurrent Pericarditis (up to 30%)
  • Myocarditis: present in up to 30% of idiopathic pericarditis

The Diagnosis

Based on at least two of the following – typical chest pain, pericardial friction rub, typical electrocardiographic changes, and pericardial effusion.

  • Differential: esophageal disorders, costochondritis, acute MI, aortic dissection, pulmonary embolus, gastritis/PUD
  • History:
    • Chest pain, usually retrosternal, sudden, and pleuritic.
    • Worse when supine, better when sitting upright and leaning forward. Can radiate to neck, arms, etc.
    • TIP: if pain radiates to the trapezius, consider pericarditis, because the phrenic nerve (which innervates parts of the pericardium) runs through this muscle. This is virtually pathognomonic.
  • Physical exam:
    • Fever: temperature above 38.5°C suggests that a specific cause is present (i.e. purulent pericarditis)
    • Friction rub: present in up to 85% of patients. High-pitched, squeaky, and best heard at the left sternal border with the patient leaning forward.
      • Present throughout the respiratory cycle (differs from pleural rubs, which stop when the patient holds their breath)
      • TIP: friction rubs can vary in intensity from moment to moment, so the exam can be different based on the time.
    • Hypotension, tachycardia, and elevated JVP: Beck’s Triad! Suggestive of cardiac tamponade.
      • Pulsus Paradoxus: see here for information on how to perform this evaluation
      • 15% of idiopathic pericarditis
      • Up to 60% of malignant, purulent, or tuberculous pericarditis
  • Electrocardiography:
    • Classic: diffuse, ST-segment elevation and PR depression – present in up to 80% of patients with pericarditis
    • 4 phases:
      • Stage I: diffuse, concave ST-segment elevation and PR depression. Stage II: normalization of the ST and PR segments
      • Stage III: diffuse T-wave inversions
      • Stage IV: normalization of the T-waves
    • ST-elevation MI v Pericarditis
      • ST-segments are concave (as opposed to the convex or dome-shaped ST-elevations seen in MI)
      • Ratio of ST-segment elevation to T-wave amplitude in lead V6 > 0.24 suggests acute pericarditis
    • Pericarditis table 2
  • CXR: apparent cardiomegaly may suggest a large effusion, but a small, rapidly accumulating effusion can be clinically significant without being apparent on XR. Important to rule out pulmonary or mediastinal disease.
  • Laboratory testing:
    • Inflammatory markers: ESR, CRP – often elevated, but do not provide significant insight regarding the etiology of the pericarditis.
    • WBC count: if significantly elevated, could suggest purulent pericarditis
    • H/H: anemia could suggest chronic inflammatory condition or malignancy
    • Troponin: elevated in 35-50% of patients with pericarditis. Typically, elevation of troponin does not suggest poor prognosis, though persistent elevation may be due to true myocarditis.
    • Testing for ANA, RF, complements, etc. should be guided by history and exam – they should not be ordered in all cases of pericarditis.
  • Echocardiography: helps to determine if there is a pericardial effusion, tamponade, or systolic dysfunction. Left-ventricular dysfunction is uncommon. Large effusions (> 20mm in width on echo) are more likely to cause tamponade, but smaller, rapidly accumulating effusions can cause tamponade without enlarging the silhouette on XR, giving additional reason for prompt echocardiographic evaluation.
  • Cardiac MRI: not typically recommended, but can be helpful in identifying because pericardial thickening, enhanced pericardial gadolinium uptake on MRI, or both support the diagnosis
  • Pericardiocentesis and Biopsy:
    • Indications:
      • Tamponade
      • Known or suspected purulent or or neoplastic effusion
    • Not a strong diagnostic tool: in patients with unknown cause for pericarditis after considering history, imaging, and lab data, pericardiocentesis and pericardial biopsy provided a diagnosis in only ~5% of cases.
    • Lab studies to be sent on pericardial fluid
      • RBC count, WBC count
      • Cytology
      • Gram stain and culture
      • PCR and ADA for TB
      • pH, glucose, LDH, protein: not specifically linked to particular etiologies

pericarditis diagnostic flow

The Treatment

  • Initial bout of pericarditis: 70 to 90% of cases resolve completely
    • NSAIDS: goal is to relieve pain and inflammation; effective in up to 90%
      • Many NSAIDs are effective: can use ASA if known CV disease or recent MI. Ibuprofen is often preferred, due to lower risk of GI side effects.
      • Indomethacin should be avoided in patients with coronary artery disease, since it diminishes coronary blood flow.
      • Patient should also be started on a PPI to reduce the risk of ulcers.
      • 1-2 week course is reasonable
      • Some suggest tapering NSAIDs and guiding therapy based on CRP, but data are lacking
    • Colchicine: significantly reduced the rate of incessant or recurrent pericarditis.
      • ICAP randomized clinical trial: NSAID + (colchicine or placebo)
        • Colchicine, as compared with placebo, resulted in a significantly lower rate of persistent or recurrent pericarditis (17% vs. 38%)
        • Lower rate of persistent symptoms at 72 hours (19% vs. 40%)
        • Effect thought to be mediated blockade of microtubule assembly in white cells
      • 3-month course is reasonable
  • Recurrent pericarditis: more common in women and in TRAPS
    • Prompt reinstitution of NSAID therapy + Colchicine
    • Poor Response
  • Persistent pericarditis: poor response is defined as “continued chest pain necessitating treatment with analgesic agents, fever, or worsening effusion despite at least 1 week of treatment.”
    • Steroids
      • ESC Guidelines (2004): initiate glucocorticoid therapy
      • Observational data: steroids can have high rate of symptom relief – but also an increased rate of recurrence!
      • Steroids appear to reduce the anti-inflammatory effects of colchicine
      • High dose regimens can increase the risk for recurrence
      • If steroids are necessary, it is preferable to use moderate doses (0.2 to 0.5 mg/kg prednisone daily for several weeks)
      • Continue NSAIDs and Colchicine for some time after steroid taper ends
    • Other Immunosuppresants: data is lacking, but there are small studies that suggest the effectiveness of medications like azathioprine, anakinra, IVIG, etc.
    • Pericardiectomy: rarely performed; not consistently effective, (? because visceral pericardium remains, along with remnants of parietal pericardium)

Pericarditis Table 1



  • Previously thought to be Pneumocystis carinii (species that infects rats) it is now known that the human pathogen is Pneumocystis jirovecii
  • Still referred to as PCP (PneumoCystis Pneumonia)
  • Fungus based on genotypic homologies
  • Incidence has greatly decreased since the use of ART and prophylaxis however still one of the leading OI in HIV pts
  • Rare cause in HIV when CD4 >200 and when bactrim ppx is taken appropriately
  • Clinical sx: Gradual onset of fever (80-100%), cough (90%) and dyspnea (95%)
  • Diagnosis: Low CD4 (95% of cases below 200), elevated LDH in 90% of patients, often hypoxic as dz progresses, CXR normal in ¼ patients or may show diffuse, bilateral, interstitial or alveolar infiltrates
  • Treatment: TMP-SMX preferred medication, if unable to take TMP-SMX then mild/mod can be tx with atovaquone or clinda/primaquine however if severe, tx with IV pentamadine
  • Steroids are recommended for PaO2 <70, AA gradient >35 or hypoxemia on pulse ox


Brain Training – does it work?


In the last several years, we have seen the rise of computer based cognitive training modules, colloquially referred to as “brain training.”  Touted as “cognitive neuroscience-based therapy,” these services aim to increase attention, memory, social skills, reasoning ability and academic skills. Questions remain, however, regarding their effectiveness. Multiple studies are often cited by the companies behind the brain training products, claiming increased cognitive abilities in as little as 4 weeks. However, a recent statement released by the Stanford University Center on Longevity and the Berlin Max Planck Institute for Human Development suggests that there is no solid scientific evidence to support these claims. Signed by leading cognitive psychologists and neuroscientists, the statement notes:

“The strong consensus of this group is that the scientific literature does not support claims that the use of software-based ‘brain games’ alters neural functioning in ways that improve general cognitive performance in everyday life, or prevent cognitive slowing and brain disease […] The promise of a magic bullet detracts from the best evidence to date, which is that cognitive health in old age reflects the long-term effects of healthy, engaged lifestyles.”

In a recent systematic review and meta-analysis, the researchers assess whether CCT programs improve cognitive test performance in cognitively healthy older adults and identify the aspects of cognition (cognitive domains) that are responsive to CCT, and the CCT design features that are most important in improving cognitive performance.


New effective interventions to attenuate age-related cognitive decline are a global priority. Computerized cognitive training (CCT) is believed to be safe and can be inexpensive, but neither its efficacy in enhancing cognitive performance in healthy older adults nor the impact of design factors on such efficacy has been systematically analyzed. Our aim therefore was to quantitatively assess whether CCT programs can enhance cognition in healthy older adults, discriminate responsive from nonresponsive cognitive domains, and identify the most salient design factors.

Methods and Findings

We systematically searched Medline, Embase, and PsycINFO for relevant studies from the databases’ inception to 9 July 2014. Eligible studies were randomized controlled trials investigating the effects of ≥4 h of CCT on performance in neuropsychological tests in older adults without dementia or other cognitive impairment. Fifty-two studies encompassing 4,885 participants were eligible. Intervention designs varied considerably, but after removal of one outlier, heterogeneity across studies was small (I2 = 29.92%). There was no systematic evidence of publication bias. The overall effect size (Hedges’ g, random effects model) for CCT versus control was small and statistically significant, g = 0.22 (95% CI 0.15 to 0.29). Small to moderate effect sizes were found for nonverbal memory, g = 0.24 (95% CI 0.09 to 0.38); verbal memory, g = 0.08 (95% CI 0.01 to 0.15); working memory (WM), g = 0.22 (95% CI 0.09 to 0.35); processing speed, g = 0.31 (95% CI 0.11 to 0.50); and visuospatial skills, g = 0.30 (95% CI 0.07 to 0.54). No significant effects were found for executive functions and attention. Moderator analyses revealed that home-based administration was ineffective compared to group-based training, and that more than three training sessions per week was ineffective versus three or fewer. There was no evidence for the effectiveness of WM training, and only weak evidence for sessions less than 30 min. These results are limited to healthy older adults, and do not address the durability of training effects.


CCT is modestly effective at improving cognitive performance in healthy older adults, but efficacy varies across cognitive domains and is largely determined by design choices. Unsupervised at-home training and training more than three times per week are specifically ineffective. Further research is required to enhance efficacy of the intervention. These findings suggest that CCT produces small improvements in cognitive performance in cognitively healthy older adults but that the efficacy of CCT varies across cognitive domains and is largely determined by design aspects of CCT. The most important result was that “do-it-yourself” CCT at home did not produce improvements. Rather, the small improvements seen were in individuals supervised by a trainer in a center and undergoing sessions 1–3 times a week. Because only cognitively healthy older adults were enrolled in the studies considered in this systematic review and meta-analysis, these findings do not necessarily apply to cognitively impaired individuals. Moreover, because all the included studies measured cognitive function immediately after CCT, these findings provide no information about the durability of the effects of CCT or about how the effects of CCT on cognitive function translate into real-life outcomes for individuals such as independence and the long-term risk of dementia.

Lampit A, Hallock H, Valenzuela M (2014) Computerized Cognitive Training in Cognitively Healthy Older Adults: A Systematic Review and Meta-Analysis of Effect Modifiers. PLoS Med 11(11): e1001756. doi:10.1371/journal.pmed.1001756

December Journal Watch


In case you missed the email, here is the December, 2014 edition of the Internal Medicine Journal Watch, curated by the IMJW editorial board (Jan Petrasek, Nico Barros, Ragisha Gopalakrishnan, Jeremy Warshauer, Shetal Patel, Ben Jenny, Vishy Lanka, Brian Davis, Ashish Gupta, and Roma Mehta). Thank you to the board for putting together this collection of important publications in science and medicine! UTSW_IMJW_12_2014

A Step Back? Medicaid Payment Cuts Looming

Although Medicaid enrollment of patients has increased with the Affordable Care Act, there is concern that less of these patients will be cared for by physicians due to changes in Medicaid payments to providers. A report from the Urban Institute estimates physicians will see their payment for primary care reduced this coming week as the enhanced payments for Medicaid  before are set to expire. With reduced compensation for taking care of Medicaid patients, many providers and organizations are worried that patients will loss access to providers and this will further discourage physicians in training to pursue primary care. Click on the links below to learn more from The New York Times and the Urban Institute.

Click to access 2000025-Reversing-the-Medicaid-Fee-Bump.pdf

#clinicalpearls Cardiology

EDITED (thank you to Dr. Khera!):

Indications for operative repair of aortic regurgitation:

  1.  CHF symptoms (OR evidence that the ventricle is decompensating)
  2. Asymptomatic, but EF 50mm (Class IIa, probably should)
  3. Asymptomatic, LV end systolic diameter > 50mm (Class IIa, probably should) – (#2 and #3 make the “rule of 50’s”)