The pericardium is the fibroelastic sac surrounding the heart. It is composed of two layers, visceral and parietal, that are separated by a "potential" space. Within this potential space, it is normal to have 15-50 mL of fluid to serve the purpose of lubrication. The term acute pericarditis refers to inflammation of this fibroelastic sac. The causes of pericarditis are wide ranging from infection, autoimmune processes, malignancy, and uremia. This article will discuss uremic pericarditis, including the etiology, epidemiology, pathophysiology, evaluation, and treatment. Uremic pericarditis typically occurs in patients with end-stage renal disease and patients with severe azotemia (elevated blood urea nitrogen, BUN), typically above 60 mg/dL. Clinical features of uremic pericarditis include chest pain, particularly in the recumbent position, a pericardial rub is often audible, and in severe cases, cardiac tamponade may be present. The diagnosis of uremic pericarditis is made by electrocardiogram which typically shows diffuse ST and T-wave elevations. Treating this condition is often by lowering BUN through dialysis.
Patients with end-stage renal disease typically have a defect in fluid and electrolyte balance leading to an accumulation of toxic metabolites such as nitrogenous wastes. In establishing a diagnosis of uremic pericarditis, studies have shown that the combination of toxic metabolite accumulation, uremic toxins, fluid overload, and electrolyte derangement contribute to the pathology. Some studies demonstrate that an increase in nitrogen waste products has a proinflammatory effect leading to pericarditis; other studies have concluded the changes in acid-base homeostasis, hypercalcemia, hyperuricemia are all implicated in the development of uremic pericarditis.
The actual incidence of uremic pericarditis is difficult to ascertain due to the variability of symptoms and varying diagnostic criteria. Various studies have reported a prevalence of 2-21% in dialysis patients.
The pathophysiology of uremic pericarditis is primarily related to the accumulation of toxic metabolites and nitrogenous waste accumulation in the blood. Research shows that these toxic metabolites provide an insult to the pericardium resulting in the release of pro-inflammatory markers such as interleukin 1, interleukin 6, and tumor necrosis factor (TNF) leading to inflammation, fibrous deposition, and adhesions causing damage to the pericardium. In severe cases, effusions can also occur in conjunction with uremic pericarditis and these can be quantified further into serous versus hemorrhagic; the cause of these pericardial effusions is multifactorial and is partially related to platelet dysfunction in renal failure patients.
A significant key finding is a patient with a history of chronic kidney disease, end-stage renal disease, or a patient receiving dialysis. Physical exam findings are variable and broad. Most patients will present with pleuritic chest pain that improves when leaning forward. Other findings can include but are not limited to fever and shortness of breath. Many of these patients will present similarly to a myocardial infarction patient, so it is essential to rule out an ischemic event in the situation.
In evaluating a patient with suspected uremic pericarditis, an electrocardiogram is necessary. Electrocardiogram findings of pericarditis include diffuse ST and T-wave elevations. To distinguish these findings from an ST-segment elevation myocardial infarction, the ST and T-wave findings in pericarditis are typically diffuse and not localized to coronary artery territory. Cardiac biomarkers may also be elevated, i.e., troponins, but are not necessary to make the diagnosis. A chest x-ray can reveal an increased cardiac silhouette which may represent an effusion. An echocardiogram is also very important to confirm or further evaluate the severity of uremic pericarditis. The echocardiogram will reveal a restrictive pattern due to the stiffness of the fibrous pericardium as a result of adhesions. In up to 50% of uremic pericarditis, pericardial effusion is noticeable on the echocardiogram. It is also important to note that pericarditis is primarily a clinical diagnosis; lab work and imaging will help aid the diagnosis but are not necessary to make the diagnosis.
Initial treatment for pericarditis has multiple options. The preferred method is to institute dialysis. Uremic pericarditis has been shown to respond rapidly to dialysis leading to resolution of chest pain as well as the pericardial effusion in about 76% of cases. The use of anti-inflammatory agents and steroids have been used but been shown to provide limited success. Anti-inflammatories such as indomethacin may provide some relief for pain but has not been shown to be successful in eliminating uremic pericarditis. The use of colchicine has been shown to be effective in treating other causes of pericarditis but has not been studied in uremic pericarditis. The use of steroids has been controversial in that it does provide relief but it also increases the risk of recurrence along with potential side effects such as hyperglycemia, the risk of osteoporosis, and neurologic effects in the elderly. Intrapericardial steroid injections have also been studies but due to the risk hemothorax, infection, pneumothorax, cardiac arrhythmia, and pneumopericardium, this approach is rarely used. If there is treatment failure with dialysis, it is recommended one perform pericardiocentesis in patients with uremic pericarditis with effusion within 7-14 days. In patients with severe uremic pericarditis and effusion leading to cardiac tamponade, emergent pericardiocentesis is recommended.
Pericardiectomy is typically not the first line and only utilized for recurrent pericarditis with pericardial effusions. Recommendations are to pursue echocardiogram every 3-5 days during the acute event to monitor pericarditis and effusion resolution.
The differential diagnosis for uremic pericarditis is broad. Pericarditis has many different etiologies, and they must all be ruled out before making the diagnosis. Although uremic pericarditis is the most common form of pericarditis in end-stage renal disease and dialysis patients, other causes merit consideration and appropriate evaluation. These other causes include infectious (viral, bacterial, fungal), inflammatory (systemic lupus erythematosus, scleroderma, vasculitis), metabolic (hypothyroidism), neoplastic (primary or metastatic), trauma (blunt or penetrating), cardiac (postpericardiotomy syndrome), and medication-induced (i.e., hydralazine, methyldopa, procainamide, minoxidil).
Overall, the resolution of uremic pericarditis is excellent, seen in 85-90% of patients. However, the risk of recurrent becomes more likely with every episode of pericarditis.
The major life-threatening complication of uremic pericarditis is the development of cardiac tamponade. If a rapid pericardial effusion accompanies uremic pericarditis, this has the potential to prevent the heart from functioning in pumping blood to the rest of the body. The increased pressure in the pericardium will create resistance to the heart from contracting and pumping blood. A typical presentation of cardiac tamponade includes hypotension, increased jugular venous distension, pulsus paradoxus, and distant heart sounds. An EKG may show electrical alternans which is a discrepancy in voltage caused by the heart floating within the pericardium due to the effusion. The treatment for this is emergent pericardiocentesis.
As part of a health professional team, it is vital to be cognizant of the potential various differential diagnoses in a patient complaining of chest pain. Although uremic pericarditis is easily treatable, grave diagnoses such as, but not limited to, ST-segment myocardial infarction, cardiac arrhythmias, aortic dissection, coronary artery dissection, and stent thrombosis must be ruled out before making the clinical diagnosis of uremic pericarditis. Since the presentation of uremic pericarditis can be consistent with STEMI (chest pain, elevated troponin, EKG findings), it is imperative to an adequate and thorough evaluation for every patient.
|||Bentata Y,Hamdi F,Chemlal A,Haddiya I,Ismaili N,El Ouafi N, Uremic pericarditis in patients with End Stage Renal Disease: Prevalence, symptoms and outcome in 2017. The American journal of emergency medicine. 2018 Mar [PubMed PMID: 29248269]|
|||Dad T,Sarnak MJ, Pericarditis and Pericardial Effusions in End-Stage Renal Disease. Seminars in dialysis. 2016 Sep [PubMed PMID: 27228946]|
|||Awan A,Tiruneh F,Wessly P,Khan A,Iftikhar H,Barned S,Larbi D, Acute Pericarditis: Descriptive Study and Etiology Determination in a Predominantly African American Population. Cureus. 2017 Jul 6 [PubMed PMID: 28924519]|
|||Rehman KA,Betancor J,Xu B,Kumar A,Rivas CG,Sato K,Wong LP,Asher CR,Klein AL, Uremic pericarditis, pericardial effusion, and constrictive pericarditis in end-stage renal disease: Insights and pathophysiology. Clinical cardiology. 2017 Oct [PubMed PMID: 28873222]|
|||Long B,Koyfman A,Lee CM, Emergency medicine evaluation and management of the end stage renal disease patient. The American journal of emergency medicine. 2017 Dec [PubMed PMID: 28893450]|
|||Restrepo D,Vaduganathan M,Fenves AZ, Uremic Pericarditis: Distinguishing Features in a Now-Uncommon Clinical Syndrome. Southern medical journal. 2018 Dec [PubMed PMID: 30512129]|