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Wednesday Morning ConferenceWednesday Morning ConferenceDecember 14December 14thth 2005 2005
Kenneth Saland M.D. FACCKenneth Saland M.D. FACC
Case PresentationCase Presentation 43 y/o white man43 y/o white man
Chief complaint(s)Chief complaint(s)
Intermittant abdominal painIntermittant abdominal pain
BloatingBloating
History of present illnessHistory of present illness
3 mos of abdominal pain-intermittent3 mos of abdominal pain-intermittent
BloatingBloating
Loose bowel movements Loose bowel movements
More recently swelling in lower extremitiesMore recently swelling in lower extremities
Weight loss of 20 lbsWeight loss of 20 lbs
PMHPMH BPHBPH
AllergyAllergy NoneNone
SHSH No tobacco, married, 1 daughter a/wNo tobacco, married, 1 daughter a/w No IVDANo IVDA Anabolic steroids in early 1990’s Anabolic steroids in early 1990’s Drinks 2-3 alcoholic drinks per monthDrinks 2-3 alcoholic drinks per month Busy engineerBusy engineer
PSHPSH Nasal surgeryNasal surgery Squamous ca lesion removed rt shoulder 1980Squamous ca lesion removed rt shoulder 1980
MedsMeds NoneNone
FHFH Both parents deceasedBoth parents deceased Mother with breast CA, father had duodenal CAMother with breast CA, father had duodenal CA No cardiac historyNo cardiac history
Review of SystemsReview of Systems
Wt loss, fatigue, poor appetiteWt loss, fatigue, poor appetite
Dyspnea on exertionDyspnea on exertion
No chest pain No chest pain
Palpitations intermittantlyPalpitations intermittantly
Loose stoolsLoose stools
Physical ExamPhysical Exam
Bp 120/60 HR 100 regular RR-22 sat 98% RABp 120/60 HR 100 regular RR-22 sat 98% RA
Wt 100 kg Height 6’3”Wt 100 kg Height 6’3”
Marked JVD Marked JVD
Clear lungsClear lungs
Tachycardic, regular no murmursTachycardic, regular no murmurs
AbdomenAbdomen
Mild generalized tendernessMild generalized tenderness
Positive bowel sounds Positive bowel sounds
No hepatosplenomegaly notedNo hepatosplenomegaly noted
Distended and edematousDistended and edematous
Extremities –trace peripheral edemaExtremities –trace peripheral edema Neuro-grossly normalNeuro-grossly normal
EKG: atrial flutter with rate of 100EKG: atrial flutter with rate of 100
CXR-normal heart size, clear lung fieldsCXR-normal heart size, clear lung fields
LabsLabs wbc-5.7wbc-5.7
Hgb-12 Hgb-12
Platelets-257Platelets-257
Cr-1.0 Na 141 K 4.5 CO2 26 Ca 9.6 Cr-1.0 Na 141 K 4.5 CO2 26 Ca 9.6
Albumin 4.2, INR 1.3 AST 16 ALT 12 AP 94 total bilirubinAlbumin 4.2, INR 1.3 AST 16 ALT 12 AP 94 total bilirubin 0.9, total globulin 2.90.9, total globulin 2.9
Hep A,B,C negative, negative PPDHep A,B,C negative, negative PPD
TSH 2.3TSH 2.3
Ferritin 276 PSA 0.3 Ferritin 276 PSA 0.3
LabsLabs Stool studies grew out dientamoeba fragilisStool studies grew out dientamoeba fragilis Ultasound of abdomen—ascitesUltasound of abdomen—ascites
Paracentesis of ascitic fluid demostrated a high Paracentesis of ascitic fluid demostrated a high SAAG of 2.2 (Serum Albumin-4.2 Ascites Albumin SAAG of 2.2 (Serum Albumin-4.2 Ascites Albumin 2.0)2.0)
Spontaneous bacterial peritonitis diagnosed with Spontaneous bacterial peritonitis diagnosed with wbcs of 2,125 97% polyswbcs of 2,125 97% polys
Ascites cytology was negativeAscites cytology was negative
EGD, Colonscopy was plannedEGD, Colonscopy was planned
Differential DxDifferential Dx SAAGSAAG
Serum-to-ascites albumin gradient: Runyon et al (1992)
>=1.1g/dLCirrhosisAlcoholic Hepatitis CHFMassive hepatic metastasesVascular occlusionFatty liver disease of pregnancyMyxedema
<1.1 g/dlPeritoneal carcinomatosisNephrotic syndromePeritoneal TBPancreatitisBowel obst/per/infarctserositis
EchocardiographyEchocardiography
Normal ejection fractionNormal ejection fraction
Mild to moderate MRMild to moderate MR
LA upper limits of normalLA upper limits of normal
No pericardial effusionNo pericardial effusion
CT of chest and abdomenCT of chest and abdomen
Ascites, prominent liver and spleenAscites, prominent liver and spleen
No signs of cirrhosis or liver massNo signs of cirrhosis or liver mass
Chest CT revealed pericardial calcificationChest CT revealed pericardial calcification
Pericardial calcification
Right Heart CatheterizationRight Heart Catheterization Cardiac output 5.0 liters/minCardiac output 5.0 liters/min
RA 24/23 mmHgRA 24/23 mmHg
RV 40/25 mmHgRV 40/25 mmHg
PA 42/27 mm HgPA 42/27 mm Hg
PCW 27/25 mmHgPCW 27/25 mmHg
LV/LVEDP 100/23 mmHgLV/LVEDP 100/23 mmHg
LV/RV simultaneous tracing reveals equilibrium of diastolic pressures
Dip and plateau configuration of the ventricular waveforms
One month later….One month later….
Surgical pathology of pericardiumSurgical pathology of pericardium
Dense fibrosis and scattered chronic Dense fibrosis and scattered chronic inflammationinflammation
Constrictive PericarditisConstrictive Pericarditis
Heavily fibrosed or calcified pericardium restricts Heavily fibrosed or calcified pericardium restricts diastolic filling and results in elevation and diastolic filling and results in elevation and equilibrium of diastolic pressures of all four equilibrium of diastolic pressures of all four chambers of the heartchambers of the heart
Usually begins with initial episode of acute Usually begins with initial episode of acute pericarditis which may not be detectable clinicallypericarditis which may not be detectable clinically
Initial fibrin deposition often with pericardial Initial fibrin deposition often with pericardial effusioneffusion
Slowly progresses to a subacute stageSlowly progresses to a subacute stage
Organization and resorption of effusionOrganization and resorption of effusion
Chronic stage of fibrous scarring and thickeningChronic stage of fibrous scarring and thickening
Obliteration of pericardial space-majority of cases Obliteration of pericardial space-majority of cases visceral and parietal layers fusevisceral and parietal layers fuse
Disease progressionDisease progression Increase in systemic venous pressure-initially Increase in systemic venous pressure-initially
maintains diastolic filling of the ventriclesmaintains diastolic filling of the ventricles
Ultimately results in renal retention of sodium and Ultimately results in renal retention of sodium and water further increasing systemic venous pressurewater further increasing systemic venous pressure
Pericardial scar may reduce diastolic ventricular Pericardial scar may reduce diastolic ventricular volumesvolumes
Compensatory tachycardiaCompensatory tachycardia
Reduced cardiac output, tachycardia and elevated Reduced cardiac output, tachycardia and elevated right heart pressures may simulate myocardial failureright heart pressures may simulate myocardial failure
Systolic contraction of the ventricles and intrinsic Systolic contraction of the ventricles and intrinsic contractile state of the myocardium are usually contractile state of the myocardium are usually normalnormal
Severe cases-myocardial function may be depressed Severe cases-myocardial function may be depressed secondary to myocardial atrophy, fibrosis or secondary to myocardial atrophy, fibrosis or obliteration of the epicardial coronary arteries in the obliteration of the epicardial coronary arteries in the fibrotic scar causing ischemiafibrotic scar causing ischemia
DiagnosisDiagnosis Symptoms of systemic venous congestionSymptoms of systemic venous congestion
Edema, abdominal swelling, ascites, passive Edema, abdominal swelling, ascites, passive hepatic congestionhepatic congestion
Postprandial fullness, dyspepsia, anorexiaPostprandial fullness, dyspepsia, anorexia
If right and left heart pressures elevatedIf right and left heart pressures elevated Orthopnea, dyspnea, coughOrthopnea, dyspnea, cough
Other symptoms-fatigue,weight loss, muscle Other symptoms-fatigue,weight loss, muscle wastingwasting
Physical findingsPhysical findings Elevated JVDElevated JVD
Kussmaul’s sign-inspiratory increase in systemic Kussmaul’s sign-inspiratory increase in systemic venous pressurevenous pressure
Pulsus paradoxus is uncommon in rigid constrictive Pulsus paradoxus is uncommon in rigid constrictive pericarditis unless pericardial effusion is presentpericarditis unless pericardial effusion is present
Diastolic pericardial “knock”-early diastolic sound Diastolic pericardial “knock”-early diastolic sound often heard along the left sternal borderoften heard along the left sternal border
The knock represents sudden cessation of The knock represents sudden cessation of ventricular filling –higher frequency than S3 ventricular filling –higher frequency than S3 and may be confused with opening snap sound and may be confused with opening snap sound of mitral stenosisof mitral stenosis
Diagnostic toolsDiagnostic tools CXR-cardiac silhouette may be small, normal or enlargedCXR-cardiac silhouette may be small, normal or enlarged
Pericardial effusion-enlarged bordersPericardial effusion-enlarged borders
Calcification-helpful but does not equal percardial constrictionCalcification-helpful but does not equal percardial constriction
CT/MR-can identify pericardial thickening, dilation of vena CT/MR-can identify pericardial thickening, dilation of vena cavae and RV deformationcavae and RV deformation
***Significant pericardial constriction may occur in presence ***Significant pericardial constriction may occur in presence of diseased but minally thickened pericardiumof diseased but minally thickened pericardium
EKG –low voltage, afib, flutter, generalized T wave changes, EKG –low voltage, afib, flutter, generalized T wave changes, conduction defects…lots of stuffconduction defects…lots of stuff
echocardiographyechocardiography Pericardial thickeningPericardial thickening
Effusions/calcificationsEffusions/calcifications
““septal bounce” –abrupt displacement of of interventricular septal bounce” –abrupt displacement of of interventricular septum during early diastolic fillingseptum during early diastolic filling
Hepatic/IVC dilationHepatic/IVC dilation
Inspiratory decrease in diastolic mitral inflow and increased Inspiratory decrease in diastolic mitral inflow and increased early diastolic tricuspid inflow(opposite changes occur with early diastolic tricuspid inflow(opposite changes occur with expiration)expiration)
Respiratory variation in doppler flow patterns may also Respiratory variation in doppler flow patterns may also suggest constriction vs restriction. suggest constriction vs restriction.
Cardiac CatheterizationCardiac Catheterization Elevation and equalization of diastolic filling Elevation and equalization of diastolic filling
pressurespressures
Catheterization of both ventricles should be Catheterization of both ventricles should be performed-elevation and virtual identical performed-elevation and virtual identical (within 5mmHg) right atrial, right (within 5mmHg) right atrial, right ventricular,left atrial, and left ventricular ventricular,left atrial, and left ventricular diastolic pressuresdiastolic pressures
Right and left ventricular diastolic pressures Right and left ventricular diastolic pressures show characteristic early diastolic dip show characteristic early diastolic dip followed by a plateaufollowed by a plateau
.
Pressures in the left (LV) and right ventricle (RV) of a patient with constrictive pericarditis. During peak inspiration (arrow), there is a decrease in LV pressure and a concomitant increase in RV pressure, indicating discordance of ventricular pressures
Right atrial pressure characterized by Right atrial pressure characterized by preserved systolic x descent, a prominent early preserved systolic x descent, a prominent early y descent . A and V waves are small and equal y descent . A and V waves are small and equal in height –M or W configurationin height –M or W configuration
Varieties of constrictive pericarditisVarieties of constrictive pericarditis
Typical forms -Typical forms -chronic (calcific, rigid shell) -subacute (non-calcific, chronic (calcific, rigid shell) -subacute (non-calcific,
elastic)elastic)
Effusive-constrictive Effusive-constrictive
LocalisedLocalised
congenitalcongenital
Etiologies of constrictive pericarditisEtiologies of constrictive pericarditis
TBTB Post-surgicalPost-surgical Prior mediastinal radiationPrior mediastinal radiation Connective tissue disorders-RA, SLEConnective tissue disorders-RA, SLE Drug-induced-procainamide,hydralazine,methysergideDrug-induced-procainamide,hydralazine,methysergide NeoplasticNeoplastic Trauma-induced inflammationTrauma-induced inflammation Infectious-bacterial, fungal, parasitic,viralInfectious-bacterial, fungal, parasitic,viral Post MI, post-pericardiotomy syndromePost MI, post-pericardiotomy syndrome IdiopathicIdiopathic congenitalcongenital
Treatment and prognosisTreatment and prognosis Diet and diureticsDiet and diuretics
Avoid calcium and beta blockers because mild sinus Avoid calcium and beta blockers because mild sinus tachycardia is a compensatory mechanismtachycardia is a compensatory mechanism
Complete resection of pericardium especially at diaphragmatic Complete resection of pericardium especially at diaphragmatic ventricular contactsventricular contacts
May have excessive bleeding, technically complex. High May have excessive bleeding, technically complex. High incidence of arrythmiasincidence of arrythmias
Mortality rates 5-15%Mortality rates 5-15%
Most patients achieve NYHA class 1 or 2 after surgeryMost patients achieve NYHA class 1 or 2 after surgery
Results are better with less calcium and when performed Results are better with less calcium and when performed earlier in disease courseearlier in disease course
The end!!The end!!
Constrictive vs RestrictiveConstrictive vs Restrictive History -active pericarditis History -active pericarditis ECG absence of intraventricular conduction ECG absence of intraventricular conduction
defect defect Chest radiograph pericardial calcification Chest radiograph pericardial calcification CT/MRI thickened pericardium CT/MRI thickened pericardium Echocardiogram septal notch Echocardiogram septal notch Doppler ventricular interdependence Doppler ventricular interdependence Cardiac catheterization close equilibration of Cardiac catheterization close equilibration of
diastolic pressures diastolic pressures Biopsy absence of amyloid or other infiltrative Biopsy absence of amyloid or other infiltrative
diseasedisease