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Wednesday Morning Conference
December 14th 2005
Kenneth Saland M.D. FACC
Case Presentation
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43 y/o white man
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Chief complaint(s)
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Intermittant abdominal pain
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Bloating
History of present illness
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3 mos of abdominal pain-intermittent
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Bloating
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Loose bowel movements
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More recently swelling in lower extremities
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Weight loss of 20 lbs
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PMH
 BPH
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Allergy
 None
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SH
 No tobacco, married, 1 daughter a/w
 No IVDA
 Anabolic steroids in early 1990’s
 Drinks 2-3 alcoholic drinks per month
 Busy engineer
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PSH
 Nasal surgery
 Squamous ca lesion removed rt shoulder 1980
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Meds
 None
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FH
 Both parents deceased
 Mother with breast CA, father had duodenal CA
 No cardiac history
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Review of Systems
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Wt loss, fatigue, poor appetite
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Dyspnea on exertion
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No chest pain
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Palpitations intermittantly
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Loose stools
Physical Exam
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Bp 120/60 HR 100 regular RR-22 sat 98% RA
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Wt 100 kg Height 6’3”
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Marked JVD
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Clear lungs
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Tachycardic, regular no murmurs
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Abdomen
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Mild generalized tenderness
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Positive bowel sounds
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No hepatosplenomegaly noted
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Distended and edematous
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Extremities –trace peripheral edema
Neuro-grossly normal
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EKG: atrial flutter with rate of 100
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CXR-normal heart size, clear lung fields
Labs
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wbc-5.7
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Hgb-12
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Platelets-257
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Cr-1.0 Na 141 K 4.5 CO2 26 Ca 9.6
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Albumin 4.2, INR 1.3 AST 16 ALT 12 AP 94 total bilirubin
0.9, total globulin 2.9
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Hep A,B,C negative, negative PPD
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TSH 2.3
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Ferritin 276 PSA 0.3
Labs
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Stool studies grew out dientamoeba fragilis
Ultasound of abdomen—ascites
Paracentesis of ascitic fluid demostrated a high
SAAG of 2.2 (Serum Albumin-4.2 Ascites Albumin
2.0)
Spontaneous bacterial peritonitis diagnosed with
wbcs of 2,125 97% polys
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Ascites cytology was negative
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EGD, Colonscopy was planned
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SAAG
Differential Dx
Serum-to-ascites albumin gradient: Runyon et al (1992)
>=1.1g/dL
Cirrhosis
Alcoholic Hepatitis
CHF
Massive hepatic metastases
Vascular occlusion
Fatty liver disease of pregnancy
Myxedema
<1.1 g/dl
Peritoneal carcinomatosis
Nephrotic syndrome
Peritoneal TB
Pancreatitis
Bowel obst/per/infarct
serositis
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Echocardiography
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Normal ejection fraction
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Mild to moderate MR
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LA upper limits of normal
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No pericardial effusion
CT of chest and abdomen
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Ascites, prominent liver and spleen
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No signs of cirrhosis or liver mass
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Chest CT revealed pericardial calcification
Pericardial calcification
Right Heart Catheterization
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Cardiac output 5.0 liters/min
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RA 24/23 mmHg
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RV 40/25 mmHg
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PA 42/27 mm Hg
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PCW 27/25 mmHg
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LV/LVEDP 100/23 mmHg
LV/RV simultaneous tracing reveals equilibrium of diastolic pressures
Dip and plateau configuration of the ventricular waveforms
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One month later….
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Surgical pathology of pericardium
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Dense fibrosis and scattered chronic
inflammation
Constrictive Pericarditis
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Heavily fibrosed or calcified pericardium restricts
diastolic filling and results in elevation and
equilibrium of diastolic pressures of all four
chambers of the heart
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Usually begins with initial episode of acute
pericarditis which may not be detectable clinically
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Initial fibrin deposition often with pericardial effusion
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Slowly progresses to a subacute stage
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Organization and resorption of effusion
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Chronic stage of fibrous scarring and thickening
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Obliteration of pericardial space-majority of cases
visceral and parietal layers fuse
Disease progression
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Increase in systemic venous pressure-initially
maintains diastolic filling of the ventricles
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Ultimately results in renal retention of sodium and
water further increasing systemic venous pressure
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Pericardial scar may reduce diastolic ventricular
volumes
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Compensatory tachycardia
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Reduced cardiac output, tachycardia and elevated
right heart pressures may simulate myocardial failure
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Systolic contraction of the ventricles and intrinsic
contractile state of the myocardium are usually
normal
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Severe cases-myocardial function may be depressed
secondary to myocardial atrophy, fibrosis or
obliteration of the epicardial coronary arteries in the
fibrotic scar causing ischemia
Diagnosis
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Symptoms of systemic venous congestion
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Edema, abdominal swelling, ascites, passive
hepatic congestion
Postprandial fullness, dyspepsia, anorexia
If right and left heart pressures elevated
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Orthopnea, dyspnea, cough
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Other symptoms-fatigue,weight loss, muscle
wasting
Physical findings
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Elevated JVD
Kussmaul’s sign-inspiratory increase in systemic
venous pressure
Pulsus paradoxus is uncommon in rigid constrictive
pericarditis unless pericardial effusion is present
Diastolic pericardial “knock”-early diastolic sound
often heard along the left sternal border
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The knock represents sudden cessation of
ventricular filling –higher frequency than S3
and may be confused with opening snap sound
of mitral stenosis
Diagnostic tools
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CXR-cardiac silhouette may be small, normal or enlarged
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Pericardial effusion-enlarged borders
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Calcification-helpful but does not equal percardial constriction
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CT/MR-can identify pericardial thickening, dilation of vena
cavae and RV deformation
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***Significant pericardial constriction may occur in presence
of diseased but minally thickened pericardium
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EKG –low voltage, afib, flutter, generalized T wave changes,
conduction defects…lots of stuff
echocardiography
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Pericardial thickening
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Effusions/calcifications
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“septal bounce” –abrupt displacement of of interventricular
septum during early diastolic filling
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Hepatic/IVC dilation
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Inspiratory decrease in diastolic mitral inflow and increased
early diastolic tricuspid inflow(opposite changes occur with
expiration)
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Respiratory variation in doppler flow patterns may also
suggest constriction vs restriction.
Cardiac Catheterization
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Elevation and equalization of diastolic filling
pressures
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Catheterization of both ventricles should be
performed-elevation and virtual identical
(within 5mmHg) right atrial, right
ventricular,left atrial, and left ventricular
diastolic pressures
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Right and left ventricular diastolic pressures
show characteristic early diastolic dip followed
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
.
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Right atrial pressure characterized by
preserved systolic x descent, a prominent early
y descent . A and V waves are small and equal
in height –M or W configuration
Varieties of constrictive pericarditis
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Typical forms -chronic (calcific, rigid shell) -subacute (non-calcific,
elastic)
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Effusive-constrictive
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Localised
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congenital
Etiologies of constrictive pericarditis
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TB
Post-surgical
Prior mediastinal radiation
Connective tissue disorders-RA, SLE
Drug-induced-procainamide,hydralazine,methysergide
Neoplastic
Trauma-induced inflammation
Infectious-bacterial, fungal, parasitic,viral
Post MI, post-pericardiotomy syndrome
Idiopathic
congenital
Treatment and prognosis
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Diet and diuretics
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Avoid calcium and beta blockers because mild sinus
tachycardia is a compensatory mechanism
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Complete resection of pericardium especially at diaphragmatic
ventricular contacts
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May have excessive bleeding, technically complex. High
incidence of arrythmias
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Mortality rates 5-15%
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Most patients achieve NYHA class 1 or 2 after surgery
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Results are better with less calcium and when performed
earlier in disease course
The end!!
Constrictive vs Restrictive
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History -active pericarditis
ECG absence of intraventricular conduction
defect
Chest radiograph pericardial calcification
CT/MRI thickened pericardium
Echocardiogram septal notch
Doppler ventricular interdependence
Cardiac catheterization close equilibration of
diastolic pressures
Biopsy absence of amyloid or other infiltrative
disease