uremic pericarditis

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Good Morning…. I wish for you …Trouble as light as air, friends as sold as diamonds &

success as bright as Gold.

PericarditisPericarditisUremic & Dialysis associatedUremic & Dialysis associated

Dr. Abrar Ali KatparDr. Abrar Ali KatparResident Nephrology/MedicineKing Khalid HospitalHail, KSA

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Pericarditis

1. Sac Around the Outside of the Heart (Pericardium)2. Heart

Inflammation of the Heart Sac

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Pericardium25-35 ml -

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Functions of pericardium

• Not need to sustain the life• Physiologic functions

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Pericardial effusion occurs when excessive fluid collects in the pericardium. The fluid may press on the heart enough to limit its movement within the sac.

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Uremic & Dialysis associated Pericarditis

Particularly

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Background• Richard Bright first described 163 years ago. • The association of pericarditis with renal failure

in his landmark observation of 100 cases of patients with ‘albuminous urine’, which appeared in the Guys Hospital Report of 18361.

• Autopsy studies demonstrated pericarditis or pericardial effusion in 37 of these patients.

• This is common complication of CRF, with early management likely to have a good outcome.

• Advances in dialysis technology with early & timely management dramatically reduces prevalence.

• Prevalence is 6-10% with acute or CRF.• It is associated with significant morbidity &

occasional mortality.

Richard Bright Sept 28,1789 – Dec16,1858Born in Bristol died in Londonwas an English Physician & early pioneer in research ofKidney disease.

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By Definition • Pericarditis is a disorder caused by

inflammation of the pericardium, the serous membrane enclosing the heart and the roots of the great blood vessels.

• Fibrinous, aseptic inflammation (predominantly lymphocytic) is the hallmark of uremic pericarditis.

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Pathophysiology-1 • Uremic pericarditis results from inflammation of visceral & parietal layers of pericardium by metabolic toxins that accumulate due to renal failure.

• Other factors may be involved, because pericarditis also may occur in pt’s with CRF already on dialysis.

• Putative toxins include:• urea, creatinine,

methylguanidine, guanidinoacetate, parathyroid hormone, beta2-microglobulin, uric acid, & others.

• More than one toxin apparently may be involved.

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Pathophysiology -2

• Pathogenetic changes induced by toxins have not been explained, though a rough correlation with degree & duration of azotemia exists; BUN usually > 60 mg/dl. 

• Histopathology reveals adhesions between thickened pericardial membranes.

• May be associated with hemorrhagic or serous effusion or can overlap.

• Hemorrhagic effusions are more common due to uremia-induced platelet dysfunction.

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Pathology

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Types • Some authors distinguish between 2 types of

pericarditis. • Type (A) is Uremic pericarditisUremic pericarditis,

• Which occurs in pt’s with uremia who have never received dialysis. or with in 8 wks

• Rarely found in modern medicine. • Type (B) is Dialysis-associated pericarditisDialysis-associated pericarditis,

• Which occurs in dialysis pt’s.• Due to inadequate dialysis.• Other causes are volume overload & • Bacterial or viral infections.

Reference

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Key concepts:

• Fibrosis restricts compliance of the myocardium

• Decreased compliance leads to increased ventricular pressures.

• Increased pressures restrict ventricular filling during diastole

• Decreased EDV, hence stroke volume & cardiac output is diminished.

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Studies

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Frequency

• In KSA no record I could Find.• United States

• 6-10% pt’s with advanced RF before initiation of dialysis.

• Uremia accounts upto 20% of cases with large effusions.

• Mortality/Morbidity• Associated with significant morbidity & occasional

mortality. • Mortality 3-5% from tamponade or arrhythmias. • During dialysis, frequent monitoring of electrolytes

is helpful to detect & treat hypokalemia & hypophosphatemia.

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History

• Patients complain of • Chest pain.

• Pain characteristically is pleuritic & is worse in recumbent position, but it is relieved by leaning forward.

• Some pt’s may have fever. • Patients with sizable effusions may

present with dyspnea. • Palpitations may be the presenting

complaint.

Clinical

Reference

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Physical

• On examination, • Tachycardia• Hypotension in cases with impending

tamponade. • A pericardial friction rub is present in most

cases, but the rub may be transient. • Signs of tamponade, including:

• Inspiratory jugular venous distension• Paradoxical pulse.

• Patients may be febrile.• May present with confusion.

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Clinical features1. Chest pain (41-100%).

• Pleuritic in nature.• Located commonly in the left parasternal region

(less frequently interscapular region & rarely at apex).

• Radiation to neck & shoulders is common. 2. Cough & dyspnoea in 31 to 57%

• (dyspnoea in 93% with tamponade), 3. Malaise in 55 to 66%4. Weight loss in 40%.5. Fever most common sign 75-100%6. Chills most common sign 68%.

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7. Pericardial friction rub 59 to 100% • The sound is scratchy or grating & can be

accentuated by making the patient sit up & bend forward.

• Disappearance of the pericardial rub is not always an indication of improvement & could be due to appearance of pericardial effusion.

• Associated gallop rhythm (66%) with irregular pulse.

8. Jugular venous distension (68 to 81%), 9. Hepatomegaly (68%) 10. Hypotension (56%). 11. Signs of pericardial tamponade have been found

in 14 to 56% of patients with dialysis pericarditis.

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Recording of aortic pressure showing pulsus paradoxus. During inspiration, systolic pressure declines 20 mm Hg.

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Differential Diagnosis• Angina Pectoris• Aortic Dissection• Aortic Stenosis• Gastroesophageal Reflux Disease• Myocardial Infarction• Pulmonary Embolism• Pneumothorax

• Other Problems to Be ConsideredPericarditis may occur after renal transplantation. In this case, it may be related to uremia or infections eg,

• cytomegalovirus.• Idiopathic pericarditis• Constrictive pericarditis• Purulent pericarditis

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Laboratory Studies

• Serum BUN & S.creatinine levels are elevated (azotemia).

• Monitor S.electrolyte • Na, K, Cl, Mag, Ca,

Phosphatebecause of the increased

risk of cardiac arrhythmias

• Obtain serum CK concentrations with isoenzymes, troponin, & LDH levels in order to exclude MI.

• Blood C/S• CRP• ESR

• Obtain CBC count. Significant leukocytosis may be present with an either inflammatory or infective cause of pericarditis.

• Serially monitor Hb & Hct values.

• BT if Hb >8 g because this improves the abnormalities of hemostasis associated with uremia.

• Monitor Plt. count.

• Determine PT / aPTT &, if abnormal, correct in order to lessen the chance of developing tamponade.

Workup

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Imaging Studies

• CXR examination often reveals an enlarged boot-shaped / flask shaped cardiac profile.

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markedly enlarged cardiac silhouette & normal-appearing lung parenchyma in prepericardiocentesis (A) and postpericardiocentesis (B)

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Imaging Studies

• Ultrasonography is helpful in confirming the diagnosis, particularly if cardiac tamponade is suspected.

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• Echocardiogram• Procedure of choice• Detection of a pericardial effusion

• A large effusion can cause tamponade

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CT Scan

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Other Tests

• ECG often fails to demonstrate the diffuse ST- & T-wave elevations observed in idiopathic pericarditis because of the lack of penetration of inflammatory cells into the myocardium. 

• In fact, the presence of these changes on ECG mandates a search for an alternative cause for pericarditis.

• ECG is very useful to identify the presence of effusion & to help exclude tamponade.

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• EKG• Four stages of EKG changes

• Stage 1 • S-T elevation seen globally, but more

prominent in the precordial leads• Stage 2

• S-T segment starts to normalize and T-wave increases in amplitude

• Stage 3 • Normal S-T segments and inverted T-

waves• Stage 4

• Resolution of repolarization abnormalities

Reference

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Pericarditis

• Stage 1 PericarditisS-T elevation seen globally, but more prominent in the precordial leads

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ST segment elevation with coving or a downward convexity ("frowny" configuration) is much more likely to be due to acute injury (from acute infarction).

ST segment elevation with an upward concavity (i.e., "smiley" configuration) is usually benign (and when seen with notching of the J point in one or more leads). 

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Pericarditis resulting from uremia. Note diffuse, concave upward, ST segment elevation over all epicardial leads.

ECG

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Histologic Findings

• Adhesions are present between the pericardial membranes.

• The effusions frequently are bloody.

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sterile inflammation of mesothelial surfaces. Evidently the uremic products crystallize onthese surfaces and elicit an inflammatory reaction. Note the granulation tissue (not granulomas, there is a big difference), in the epicardial fat. The exudate is largely proteinaceous.

You're looking for the exudate and inflammatory reaction on the epicardial surface.  You will see some "organization" of the exudate.That is ingrowth of granulation tissue. But there is still very little in the way of an acute inflammatory reaction.

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Medical Care

• The development of pericarditis in pt’s with severe acute or CRF is an absolute indication for dialysis.

• In most pt’s, relief of chest pain & reduction in the size of any effusion occurs within 1-2 weeks.

• Both HD & PD are efficacious in the treatment of uremic pericarditis.• HD may cause hypotension, which may be dangerous

in the setting of tamponade. So some physicians advocate heparin-free HD to reduce the risk of intrapericardial hemorrhage.

• PD may compromise respiratory function because of the effect of intraperitoneal fluid on the diaphragm.

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Cont.

• In dialysis-associated pericarditis, an increased intensity of dialysis for 10-14 days is recommended.

• Close monitoring of fluid volume & electrolytes is mandatory to detect & correct hypophosphatemia & hypokalemia, which may occur with intensive dialysis.

• The response of dialysis-associated pericarditis is not predictable.

• In some instances, consider a switch to PD if heparin-free dialysis cannot be performed.

• NSAIDs & steroids may offer symptomatic relief but are not effective without dialysis.

• Indomethacin ameliorates fever, but it does not accelerate resolution of the effusion.

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Surgical Care

• Pericardiocentesis:• Indicated in pt’s

• With effusions > 250 mL or • Effusion increases despite intensive

dialysis for 10-14 days or • Evidence of tamponade.

• Pericardial window is a modification of balloon valvuloplasty: • In which an uninflated balloon is passed

inside the pericardial space, where it is opacified, inflated, and then pulled through the pericardium to create a window through which pericardial fluid drains into the peritoneal or pleural space.

Reference

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Surgical Care----

• Subxiphoid pericardiotomy:• Is performed under local anesthesia and has a

lower risk of complications compared to pericardiectomy. Consider subxiphoid pericardiotomy for large effusions that do not resolve.

• Pericardiectomy:• Is the most effective procedure managing large

effusions because it has the lowest associated risk of recurrent effusions.

• It requires general anesthesia & thoracotomy; therefore, should be considered only if pericardiotomy cannot be performed or has been unsuccessful.

Reference

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Treatment urgent• Cardiac tamponade

• Muffled heart sounds• JVD• RUQ pain on palpation• X-ray=large cardiac silhouette• Acute Management

• Volume expansion• 500ml-1000ml bolus

• Temporary• Pericardiocentesis

• Done in the ER if unstable• Performed in controlled setting if stable

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Consultation

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Consultations

• Consult with a cardiologist for evaluation with echocardiogram.

• Consult with a cardiothoracic surgeon for all patients with large effusions. • Development of tamponade is

unpredictable. • Hence it is important for the surgeon to

be aware of the patient if an emergent procedure is necessary.

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• Diet• Patients on dialysis require a daily diet

restricted to • 1.2 g/kg of protein, • 2 g of Na, & • 2 g of K.

• Pt’s on PD may require less stringent protein restriction.

• Activity• Limited to avoid strenuous activities or

trauma, which may increase the risk of hypotension or arrhythmias.

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Medication

The goals of pharmacotherapy are to reduce morbidity & to prevent

complications.

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• NSAID’s• May offer symptomatic relief but are ineffective

in absence of dialysis.• Corticosteroids

• May offer symptomatic relief but are ineffective in the absence of dialysis.

• Under study• Azathioprine• Colchicine

• Current data tend to favour colchicine to prevent recurrence.

• Colchicine suppressed the development of urate crystal-induced inflammation.

• dose (0.25 mg/kg)

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Drug Name

Indomethacin (Indocin)

Often considered the first choice. Rapidly absorbed, and metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation. Inhibits prostaglandin synthesis. Demonstrated to ameliorate fever but does not accelerate resolution of effusion.

Adult Dose 25-50 mg PO q6h

Pediatric Dose 1-2 mg/kg/d PO divided bid/qid; not to exceed 4 mg/kg/d or 150-200 mg/d

ContraindicationsDocumented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

pregnancy B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur; discontinue if persistent leukopenia, granulocytopenia, or thrombocytopenia occurs

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Drug NamePrednisone (Deltasone, Sterapred, Orasone)

May decrease inflammation by reversing increased capillary permeability and by suppressing PMN activity.

Adult Dose 5-60 mg/d PO or divided bid/qid, taper over 2 wk as symptoms resolve

Pediatric Dose4-5 mg/m2/d PO; alternatively, 0.05-2 mg/kg PO divided bid/qid; taper over 2 wk as symptoms resolve

ContraindicationsDocumented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease

Interactions

Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

pregnancyB - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use

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Further Inpatient Care

• Pt’s with significant effusion requiring medical or surgical therapy require admission to the hospital.Follow-up

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Further Outpatient Care

• Carefully monitor the patient at follow-up hemodialysis visits for recurrence of signs or symptoms.

• Up to 15% of patients may have recurrence of pericarditis.

Follow-up

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Transfer

• Pt’s may require transfer to a hospital setting in which hemodialysis & cardiothoracic surgery are available.Follow-up

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Deterrence/Prevention

• Early intervention with dialysis may prevent the development of uremic pericarditis.

• Maintenance of adequate dialysis therapy lessens the likelihood of a pt’s developing dialysis-associated pericarditis.

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Complications

• Pericardial tamponade • Pulsus paradoxus is an inspiratory fall

in systolic arterial BP of > 10 mm Hg. • It occurs in 70-80% of pt’s with

pericardial tamponade. • Pulsus paradoxus also occurs in pt’s

with • Severe asthma, • Constrictive pericarditis, & • Severe congestive heart failure.

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Prognosis

• Pt’s with uremic pericarditis, 3-5% may develop hemorrhagic pericarditis.

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Patient Education

• Instruct pt’s to call / approach their physician should symptoms recur.

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Medicolegal Pitfalls

• Failure to diagnose uremic pericarditis in a timely manner could result in significant morbidity & occasional mortality.

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Conclusion / summary

• Pericarditis may be the most dramatic complication of uremia because of suddenness with which it appears & hemodynamic complications that it may produce.

• Dialysis associated pericarditis cause mortality in about 8-10% of these patients.

• The most important aspect of management of these patients is adequacy of dialysis, treatment of underlying disease states & to rule out infections.

• The type of invasive pericardial procedure chosen is determined by local experience and the expertise available.

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Approach

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ReferencesAlpert MA, Ravenscraft MD. Pericardial involvement in end-stage renal disease. Am J Med Sci. Apr 2003;325(4):228-36. [Medline].Chen Y, Brennessel D, Walters J, et al. Human immunodeficiency virus-associated pericardial effusion: report of 40 cases and review of the literature. Am Heart J. Mar 1999;137(3):516-21. [Medline].Connors JP, Kleiger RE, Shaw RC, et al. The indications for pericardiectomy in the uremic pericardial effusion. Surgery. Dec 1976;80(6):689-94. [Medline].Emelife-Obi C, Chow MT, Qamar-Rohail H, et al. Use of a phosphorus-enriched hemodialysate to prevent hypophosphatemia in a patient with renal failure-related pericarditis. Clin Nephrol. Aug 1998;50(2):131-3. [Medline].Lundin AP. Recurrent uremic pericarditis: A marker of inadequate dialysis. Semin Dial. 1990;3:5.Mandell BF. Cardiovascular involvement in systemic lupus erythematosus. Semin Arthritis Rheum. Nov 1987;17(2):126-41. [Medline].Permanyer-Miralda G, Sagrista-Sauleda J, Soler-Soler J. Primary acute pericardial disease: a prospective series of 231 consecutive patients. Am J Cardiol. Oct 1 1985;56(10):623-30. [Medline].Rostand SG, Rutsky EA. Pericarditis in end-stage renal disease. Cardiol Clin. Nov 1990;8(4):701-7. [Medline].Sever MS, Steinmuller DR, Hayes JM, et al. Pericarditis following renal transplantation. Transplantation. Jun 1991;51(6):1229-32. [Medline].Shimojo H, Nishiue T, Yamamoto S, et al. [Uremic pericarditis complicating cardiac tamponade: a case report]. J Cardiol. Jul 2004;44(1):27-31. [Medline].Singh NP, Prakash A, Makhija A, et al. Staphylococcal pericarditis in a chronic renal failure patient. Ren Fail. May 2003;25(3):493-8. [Medline].Spector D, Alfred H, Siedlecki M, et al. A controlled study of the effect of indomethacin in uremic pericarditis. Kidney Int. Nov 1983;24(5):663-9. [Medline].Stewart JR, Fajardo LF, Gillette SM, et al. Radiation injury to the heart. Int J Radiat Oncol Biol Phys. Mar 30 1995;31(5):1205-11. [Medline].Zakynthinos E, Theodorakopoulou M, Daniil Z, et al. Hemorrhagic cardiac tamponade in critically ill patients with acute renal failure. Heart Lung. Jan-Feb 2004;33(1):55-60. [Medline].Zayas R, Anguita M, Torres F, et al. Incidence of specific etiology and role of methods for specific etiologic diagnosis of primary acute pericarditis. Am J Cardiol. Feb 15 1995;75(5):378-82. [Medline].

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Questions?

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